异氟醚、卡托普利联合预处理对兔心肌缺血再灌注损伤保护作用的研究
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摘要
目的建立缺血再灌注模型,观察异氟醚、卡托普利联合预处理对兔缺血再灌注的心肌保护作用。
方法健康新西兰大白兔,采用结扎冠状动脉左前降支法制备心肌缺血再灌注模型。随机分成6组：假手术组(S组)：仅开胸并分离冠状动脉左前降支,但不阻断血流；缺血再灌注组(I/R组)：缺血30min,再灌注120 mim缺血预处理组(IPC组)：缺血5 min,再灌注5 min,重复3次后同I/R处理；异氟醚预处理组(I组)：给予1.1%异氟醚持续吸入30min,洗脱15min,之后处理同I/R组；卡托普利预处理组(C组)：给予喂饲卡托普利片25 mg-kg-1,24h后处理同I/R组；异氟醚、卡托普利联合预处理组(I+C组)：给予喂饲卡托普利片25 mg·kg-1,24h后处理同I组。记录缺血再灌注前后不同时间点血流动力学指标：阻断前(T0),阻断30min(T1),再灌注30min(T2),再灌注60min(T3),再灌注120min(T4)；记录心律失常发生率；取动脉血检测乳酸脱氢酶(LDH)、肌酸磷酸激酶(CK)、肌酸磷酸激酶同工酶(CK-MB)、心肌肌钙蛋白(cTnI)浓度；再灌注结束后检测血清丙二醛(MDA)浓度及超氧化物歧化酶(SOD)活性；观察各组心肌细胞超微结构变化。
结果1.T0-T2 I组与I+C组HR相对高于其它各组,T0-T4 I组、C组与I+C组MAP与RPP相对较低并依次递减(P<0.05,或P<0.01),IPC组、I组、C组再灌注期间心律失常发生率(37.5%、50%、50%)低于I/R组(62.5%),但高于I+C组(25%,P<0.05)。2.心肌酶变化：与S组比,各组心肌酶学指标从T1至T4均较T0有所升高(P<0.05或P<0.01),但IPC组、I组、C组和I+C组增高程度低于I/R(P<0.05),IPC组和I+C组又较I组和C组低(P<0.05)。3.生化指标变化：与S组比,各组MDA均增高,SOD降低(P<0.01),但与I/R组比,各处理组MDA降低,SOD较高(P<0.01)。IPC组和I+C组MDA和SOD分别较I组和C组降低和升高(P<0.05)。4.心肌超微结构变化：预处理组心肌细胞损伤轻于I/R组。
结论异氟醚、卡托普利联合预处理对缺血再灌注兔心肌有保护作用,较单独应用异氟醚、卡托普利预处理的保护作用增强,其效果与缺血预处理相似。
目的建立缺血再灌注模型,观察异氟醚、卡托普利联合预处理对兔心肌细胞凋亡的影响。
方法健康新西兰大白兔,采用结扎冠状动脉左前降支法制备心肌缺血再灌注模型。随机分成6组：假手术组(S组)：仅开胸并分离冠状动脉左前降支,但不阻断血流；缺血再灌注组(I/R组)：缺血30min,再灌注120 min；缺血预处理组(IPC组)：缺血5 min,再灌注5 min,重复3次后处理同I/R组；异氟醚预处理组(I组)：给予1.1%异氟醚持续吸入30min,洗脱15min,之后处理同I/R组；卡托普利预处理组(C组)：给予喂饲卡托普利片25 mg·kg-1,24h后处理同I/R组；异氟醚、卡托普利联合预处理组(I+C组)：给予喂饲卡托普利片25 mg·kg-1,24h后处理同I组。再灌注结束后采用伊文思蓝和TTC染色法检测心肌梗死面积,流式细胞仪检测细胞凋亡的情况。
结果1.心肌梗死面积：IPC组、I组、C组和I+C组心肌梗死面积(33.6±3.8%、39.8±5.7%、39.6±3.4%、33.9±5.9%)均小于I/R组(60.7±6.0)(P<0.01),IPC、I+C组心肌梗死面积均小于I组、C组(P<0.05)。2.细胞凋亡：与S组比较各组凋亡指数明显增高(P＜0.01)；与I/R组相比各预处理组细胞凋亡指数均有所降低(P<0.01)；I组和C组较IPC组和I+C组细胞凋亡指数有所增加(P<0.05)。但IPC组和I+C组之间,差异无统计学意义(P＜0.05)。
结论1.异氟醚、卡托普利联合预处理可明显减少心肌缺血再灌注的梗死面积以及降低细胞凋亡,较单独药物预处理组作用增强,与缺血预处理的作用相似。2.异氟醚、卡托普利联合预处理对心肌缺血再灌注损伤产生了协同的抗细胞凋亡保护作用。
目的建立缺血再灌注模型,初步探讨异氟醚、卡托普利联合预处理对凋亡相关基因的影响,以及对凋亡通路的作用机制。
方法健康新西兰大白兔,采用结扎冠状动脉左前降支法制备心肌缺血再灌注模型。随机分成6组：假手术组(S组)：仅开胸并分离冠状动脉左前降支,但不阻断血流；缺血再灌注组(I/R组)：缺血30min,再灌注120 mim缺血预处理组(IPC组)：缺血5 min,再灌注5 min,重复3次后处理同I/R组；异氟醚预处理组(I组)：给予1.1%异氟醚持续吸入30min,洗脱15min,之后处理同I/R组；卡托普利预处理组(C组)：给予喂饲卡托普利片25mg·kg-1,24h后处理同I/R组；异氟醚、卡托普利联合预处理组(I+C组)：给予喂饲卡托普利片25mg·kg-1,24h后处理同I组。再灌注结束后采用免疫印迹法(Western-Blot)检测各组心肌凋亡相关基因Bcl-2、Bax和凋亡通路蛋白Caspase-3、Caspase-8和Caspase-9的表达,流式细胞仪检测细胞凋亡的情况。
结果1.各组心肌Bcl-2、Bax蛋白表达的变化：与I/R组比较,各预处理组Bcl-2表达明显增加,Bax表达降低,Bcl-2/Bax比值明显增加,差异有显著统计学意义(P<0.01)；与I组和C组相比,IPC组和I+C组Bcl-2/Bax比值明显增高(P<0.01),IPC组和I+C组之间比值没有差异(P>0.05)。2.各组心肌凋亡通路蛋白Caspase-3、Caspase-8和Caspase-9蛋白表达的变化：与I/R组比较各预处理组Caspase-3、Caspase-8和Caspase-9蛋白表达明显降低,差异有显著统计学意义(P<0.01)；与I组和C组相比,IPC组Caspase-3蛋白表达较低(P<0.01),但与I+C组相比差别无统计学意义(P>0.05)；各药物预处理组Caspase-8蛋白表达与IPC组相比均较低(P<0.05或P<0.01)；I+C组Caspase-8蛋白的表达量也低于I组和C组(P<0.01)；与各药物预处理组相比,IPC组的Caspase-9蛋白表达较低(P<0.01)；I+C组与I组和C组相比,Caspase-9蛋白的表达量也有差异(P<0.05)。3.细胞凋亡：与I/R组相比,各预处理组细胞凋亡指数均有所降低(P<0.01),I+C组凋亡指数低于I组和C组(P<0.05),但与IPC组无差异(P>0.05)
结论1.异氟醚、卡托普利联合预处理组通过上调Bcl-2蛋白表达,下调Bax蛋白表达,增加Bcl-2/Bax比值,对缺血再灌注兔心肌产生保护作用。2.异氟醚、卡托普利联合预处理组降低心肌缺血再灌注后Caspase-3、Caspase-8和Caspase-9的蛋白表达,抑制凋亡通路信号转导,减少心肌细胞的凋亡。3.异氟醚、卡托普利联合预处理对凋亡的死亡受体通路和线粒体通路具有抑制作用,但主要是通过死亡受体通路发挥抗凋亡作用。
Objective:To investigate the cardioprotective effect of the combina-tion of isoflurane and captopril preconditioning on myocardial ischemia reperfusion injury in rabbit.
Methods:All healthy New Zealand white rabbits were randomly assigned to six groups (n=8 each):(1) Sham-operated group(group S), rabbits were opened chest without ligating the left anterior descending coronary artery (LAD); (2) Ischemia/reperfusion group (group I/R) group; (3) Ischemic preconditioning group (group IPC),5min ischemia-5min reperfusion for three cycles before the long time ischemia; (4) Isoflurane group (groupⅠ), rabbits were pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout; (5) Captopril group(group C), rabbits were feeded captopril tablets (25 mg·kg-1) before 24h; (6) Combination of isoflurane and captopril preconditioning group(group I+C), rabbits were feeded captopril tablets (25mg·kg-1) before 24h and pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout after 24h. After preconditioning, all rabitts were treated 30min of ischemia and 2h of reperfusion except for group S. Hemodynamic parameters and incidence rate of arrhythmia were recorded at before ischemia (To),30min after ischemia (T1),30min after reperfusion(T2),60min after reperfusion(T3) and 120min after reperfusion(T4). Blood samples were taken from arterial line for determination of plasma CK, CK-MB, LDH and cTnI levels. At the end of the reperfusion, the plasma concentration of MDA and activity of SOD were examined and myocardial structure was observed under light and electron microscope.
Results:Heart Rate(HR) of group I+C was significantly higher than other groups and Mean Arterial Pressure (MAP) was lower (P<0.05 or P＜0.01). And incidence rate of arrhythmia was lower in group I+C (P＜0.05). The CK, CKMB, LDH and cTnI levels of group IPC and group I+C were significantly lower than that of groupⅠ, group C and group I/R (P＜0.05), but were higher than group S (P＜0.05). The injury of group I/R was worse than the others from the changes of the cellular structure under light and electron microscope. Group IPC and group I+C had lower concentration of MDA and also had higher activity of SOD than other groups except for group S.
Conclusions:The combination of isoflurane and captopril pre-conditioning induces cardioprotection against ischemia reperfusion injury in rabbits. The cardioprotection was better than that of solitary preconditioning and similar with that of group IPC.
Objective:To investigate the effect of the combination of isoflurane and captopril preconditioning on myocardial infarct size(IS) and apoptosis during ischemia-reperfusion in rabbit.
Methods:All healthy New Zealand white rabbits were randomly assigned to six groups(n=8 each):(1) Sham-operated group(group S), rabbits were opened chest without ligating the left anterior descending coronary artery; (2) Ischemia/reperfusion group(group I/R); (3) Ischemic preconditioning group(group IPC),5min ischemia-5min reperfusion for three cycles before the long time ischemia; (4) Isoflurane group (groupⅠ), rabbits were pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout; (5) Captopril group(group C), rabbits were feeded captopril tablets (25mg·kg-1) before 24h; (6) Combination of isoflurane and captopril preconditioning group(group I+C), rabbits were feeded captopril tablets (25mg·kg-1) before 24h and pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout after 24h. After preconditioning, all rabitts were treated 30min of ischemia and 2h of reperfusion except for group S. At the end of the reperfusion, infarct size(IS) and area at risk(AAR) were accessde by Evans Blue and TTC staining. Apotosis index were detected by flow cytometry.
Results:Myocardial infarct size of group IPC, groupⅠ, group C and group I+C (33.6±3.8%,39.8±5.7%,39.6±3.4%,33.9±5.9%) were less than that of group I/R (60.7±6.0, P<0.01). Myocardial infarct size of group IPC and group I+C were less than that of groupⅠand group C (P<0.05), but distinction between group IPC and group I+C was not significantly (P>0.05). Apoptotic index of group S was the lowest in eath group (P＜0.01). Apoptotic index of group I/R was less than that of group IPC, group I, group C and group I+C(P<0.01). Apoptotic index of group I+C was less than that of groupⅠand group C, but not different with that of group IPC (P＜0.05).
Conclusions:The combination of isoflurane and captopril preconditioning can reduce myocardial infarct size and the incidence rate of apoptotic during ischemia reperfusion in rabbits. The effect was better than that of solitary preconditioning and similar with that of group IPC. The combination of isoflurane and captopril preconditioning produced a synergistic protective effect of anti-apoptosis.
Objective:To investigate the effect of the combination of isoflurane and captopril preconditioning on apoptosis-related gene and apoptosis pathway during myocardial ischemia and reperfusion in rabbit.
Methods:All healthy New Zealand white rabbits were randomly assigned to six groups (n=8 each):(1) Sham-operated group(group S), rabbits were opened chest without ligating the left anterior descending coronary artery; (2) Ischemia/reperfusion group(group I/R); (3) Ischemic preconditioning group (group IPC),5min ischemia-5min reperfusion for three cycles before the long time ischemia; (4) Isoflurane group (groupⅠ), rabbits were pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout; (5) Captopril group (group C), rabbits were feeded captopril tablets (25 mg·kg-1) before 24h; (6) Combination of isoflurane and captopril preconditioning group (group I+C), rabbits were feeded captopril tablets (25 mg·kg-1) before 24h and pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout after 24h. After preconditioning, all rabitts were treated 30min of ischemia and 2h of reperfusion except for group S. At the end of the reperfusion, the heart was harvested and the activity of apoptosis-related gene (Bcl-2 and Bax) and apoptosis pathway proteins (caspase-3, caspase-8 and caspase-9) were determined by Western Blot analysis, apotosis index was detected by flow cytometry.
Results:Bcl-2/Bax ratio of group I+C and group IPC was higher than that of groupⅠand group C (P<0.01). But Bcl-2/Bax ratio of group I+C was the same high as that of group IPC. The activity of caspase-3, caspase-8 and caspase-9 of every preconditioning group were lower than that of group I/R. The activity of caspase-8 of group I+C was lower than that of other preconditioning group. The activity of caspase-9 of group IPC was lower than that of drug preconditioning group. Apotosis index of every preconditioning group was lower that of group I/R(P<0.01). Apotosis index of group I+C was lower that that of group I and group C, but ot different with that of group IPC (P>0.05).
Conclusions:The combination of isoflurane and captopril preconditioning can promote the activity of Bcl-2, inhibit the activity of Bax and increase Bcl-2/Bax ratio in myocardium during ischemia reperfusion, which maybe one of molecular mechanisms of the combina-tion of isoflurane and captopril preconditioning on cardioprotection. The combination of isoflurane and captopril preconditioning can inhibit the activity of caspase-3, caspase-8 and caspase-9 and signal transduction of apoptosis pathway, which indicate that the combination of isoflurane and captopril preconditioning can inhibit mitochondrion pathway and death receptor pathway, but mainly the latter.
方法健康新西兰大白兔,采用结扎冠状动脉左前降支法制备心肌缺血再灌注模型。随机分成6组：假手术组(S组)：仅开胸并分离冠状动脉左前降支,但不阻断血流；缺血再灌注组(I/R组)：缺血30min,再灌注120 mim缺血预处理组(IPC组)：缺血5 min,再灌注5 min,重复3次后同I/R处理；异氟醚预处理组(I组)：给予1.1%异氟醚持续吸入30min,洗脱15min,之后处理同I/R组；卡托普利预处理组(C组)：给予喂饲卡托普利片25 mg-kg-1,24h后处理同I/R组；异氟醚、卡托普利联合预处理组(I+C组)：给予喂饲卡托普利片25 mg·kg-1,24h后处理同I组。记录缺血再灌注前后不同时间点血流动力学指标：阻断前(T0),阻断30min(T1),再灌注30min(T2),再灌注60min(T3),再灌注120min(T4)；记录心律失常发生率；取动脉血检测乳酸脱氢酶(LDH)、肌酸磷酸激酶(CK)、肌酸磷酸激酶同工酶(CK-MB)、心肌肌钙蛋白(cTnI)浓度；再灌注结束后检测血清丙二醛(MDA)浓度及超氧化物歧化酶(SOD)活性；观察各组心肌细胞超微结构变化。
结果1.T0-T2 I组与I+C组HR相对高于其它各组,T0-T4 I组、C组与I+C组MAP与RPP相对较低并依次递减(P<0.05,或P<0.01),IPC组、I组、C组再灌注期间心律失常发生率(37.5%、50%、50%)低于I/R组(62.5%),但高于I+C组(25%,P<0.05)。2.心肌酶变化：与S组比,各组心肌酶学指标从T1至T4均较T0有所升高(P<0.05或P<0.01),但IPC组、I组、C组和I+C组增高程度低于I/R(P<0.05),IPC组和I+C组又较I组和C组低(P<0.05)。3.生化指标变化：与S组比,各组MDA均增高,SOD降低(P<0.01),但与I/R组比,各处理组MDA降低,SOD较高(P<0.01)。IPC组和I+C组MDA和SOD分别较I组和C组降低和升高(P<0.05)。4.心肌超微结构变化：预处理组心肌细胞损伤轻于I/R组。
结论异氟醚、卡托普利联合预处理对缺血再灌注兔心肌有保护作用,较单独应用异氟醚、卡托普利预处理的保护作用增强,其效果与缺血预处理相似。
目的建立缺血再灌注模型,观察异氟醚、卡托普利联合预处理对兔心肌细胞凋亡的影响。
方法健康新西兰大白兔,采用结扎冠状动脉左前降支法制备心肌缺血再灌注模型。随机分成6组：假手术组(S组)：仅开胸并分离冠状动脉左前降支,但不阻断血流；缺血再灌注组(I/R组)：缺血30min,再灌注120 min；缺血预处理组(IPC组)：缺血5 min,再灌注5 min,重复3次后处理同I/R组；异氟醚预处理组(I组)：给予1.1%异氟醚持续吸入30min,洗脱15min,之后处理同I/R组；卡托普利预处理组(C组)：给予喂饲卡托普利片25 mg·kg-1,24h后处理同I/R组；异氟醚、卡托普利联合预处理组(I+C组)：给予喂饲卡托普利片25 mg·kg-1,24h后处理同I组。再灌注结束后采用伊文思蓝和TTC染色法检测心肌梗死面积,流式细胞仪检测细胞凋亡的情况。
结果1.心肌梗死面积：IPC组、I组、C组和I+C组心肌梗死面积(33.6±3.8%、39.8±5.7%、39.6±3.4%、33.9±5.9%)均小于I/R组(60.7±6.0)(P<0.01),IPC、I+C组心肌梗死面积均小于I组、C组(P<0.05)。2.细胞凋亡：与S组比较各组凋亡指数明显增高(P＜0.01)；与I/R组相比各预处理组细胞凋亡指数均有所降低(P<0.01)；I组和C组较IPC组和I+C组细胞凋亡指数有所增加(P<0.05)。但IPC组和I+C组之间,差异无统计学意义(P＜0.05)。
结论1.异氟醚、卡托普利联合预处理可明显减少心肌缺血再灌注的梗死面积以及降低细胞凋亡,较单独药物预处理组作用增强,与缺血预处理的作用相似。2.异氟醚、卡托普利联合预处理对心肌缺血再灌注损伤产生了协同的抗细胞凋亡保护作用。
目的建立缺血再灌注模型,初步探讨异氟醚、卡托普利联合预处理对凋亡相关基因的影响,以及对凋亡通路的作用机制。
方法健康新西兰大白兔,采用结扎冠状动脉左前降支法制备心肌缺血再灌注模型。随机分成6组：假手术组(S组)：仅开胸并分离冠状动脉左前降支,但不阻断血流；缺血再灌注组(I/R组)：缺血30min,再灌注120 mim缺血预处理组(IPC组)：缺血5 min,再灌注5 min,重复3次后处理同I/R组；异氟醚预处理组(I组)：给予1.1%异氟醚持续吸入30min,洗脱15min,之后处理同I/R组；卡托普利预处理组(C组)：给予喂饲卡托普利片25mg·kg-1,24h后处理同I/R组；异氟醚、卡托普利联合预处理组(I+C组)：给予喂饲卡托普利片25mg·kg-1,24h后处理同I组。再灌注结束后采用免疫印迹法(Western-Blot)检测各组心肌凋亡相关基因Bcl-2、Bax和凋亡通路蛋白Caspase-3、Caspase-8和Caspase-9的表达,流式细胞仪检测细胞凋亡的情况。
结果1.各组心肌Bcl-2、Bax蛋白表达的变化：与I/R组比较,各预处理组Bcl-2表达明显增加,Bax表达降低,Bcl-2/Bax比值明显增加,差异有显著统计学意义(P<0.01)；与I组和C组相比,IPC组和I+C组Bcl-2/Bax比值明显增高(P<0.01),IPC组和I+C组之间比值没有差异(P>0.05)。2.各组心肌凋亡通路蛋白Caspase-3、Caspase-8和Caspase-9蛋白表达的变化：与I/R组比较各预处理组Caspase-3、Caspase-8和Caspase-9蛋白表达明显降低,差异有显著统计学意义(P<0.01)；与I组和C组相比,IPC组Caspase-3蛋白表达较低(P<0.01),但与I+C组相比差别无统计学意义(P>0.05)；各药物预处理组Caspase-8蛋白表达与IPC组相比均较低(P<0.05或P<0.01)；I+C组Caspase-8蛋白的表达量也低于I组和C组(P<0.01)；与各药物预处理组相比,IPC组的Caspase-9蛋白表达较低(P<0.01)；I+C组与I组和C组相比,Caspase-9蛋白的表达量也有差异(P<0.05)。3.细胞凋亡：与I/R组相比,各预处理组细胞凋亡指数均有所降低(P<0.01),I+C组凋亡指数低于I组和C组(P<0.05),但与IPC组无差异(P>0.05)
结论1.异氟醚、卡托普利联合预处理组通过上调Bcl-2蛋白表达,下调Bax蛋白表达,增加Bcl-2/Bax比值,对缺血再灌注兔心肌产生保护作用。2.异氟醚、卡托普利联合预处理组降低心肌缺血再灌注后Caspase-3、Caspase-8和Caspase-9的蛋白表达,抑制凋亡通路信号转导,减少心肌细胞的凋亡。3.异氟醚、卡托普利联合预处理对凋亡的死亡受体通路和线粒体通路具有抑制作用,但主要是通过死亡受体通路发挥抗凋亡作用。
Objective:To investigate the cardioprotective effect of the combina-tion of isoflurane and captopril preconditioning on myocardial ischemia reperfusion injury in rabbit.
Methods:All healthy New Zealand white rabbits were randomly assigned to six groups (n=8 each):(1) Sham-operated group(group S), rabbits were opened chest without ligating the left anterior descending coronary artery (LAD); (2) Ischemia/reperfusion group (group I/R) group; (3) Ischemic preconditioning group (group IPC),5min ischemia-5min reperfusion for three cycles before the long time ischemia; (4) Isoflurane group (groupⅠ), rabbits were pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout; (5) Captopril group(group C), rabbits were feeded captopril tablets (25 mg·kg-1) before 24h; (6) Combination of isoflurane and captopril preconditioning group(group I+C), rabbits were feeded captopril tablets (25mg·kg-1) before 24h and pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout after 24h. After preconditioning, all rabitts were treated 30min of ischemia and 2h of reperfusion except for group S. Hemodynamic parameters and incidence rate of arrhythmia were recorded at before ischemia (To),30min after ischemia (T1),30min after reperfusion(T2),60min after reperfusion(T3) and 120min after reperfusion(T4). Blood samples were taken from arterial line for determination of plasma CK, CK-MB, LDH and cTnI levels. At the end of the reperfusion, the plasma concentration of MDA and activity of SOD were examined and myocardial structure was observed under light and electron microscope.
Results:Heart Rate(HR) of group I+C was significantly higher than other groups and Mean Arterial Pressure (MAP) was lower (P<0.05 or P＜0.01). And incidence rate of arrhythmia was lower in group I+C (P＜0.05). The CK, CKMB, LDH and cTnI levels of group IPC and group I+C were significantly lower than that of groupⅠ, group C and group I/R (P＜0.05), but were higher than group S (P＜0.05). The injury of group I/R was worse than the others from the changes of the cellular structure under light and electron microscope. Group IPC and group I+C had lower concentration of MDA and also had higher activity of SOD than other groups except for group S.
Conclusions:The combination of isoflurane and captopril pre-conditioning induces cardioprotection against ischemia reperfusion injury in rabbits. The cardioprotection was better than that of solitary preconditioning and similar with that of group IPC.
Objective:To investigate the effect of the combination of isoflurane and captopril preconditioning on myocardial infarct size(IS) and apoptosis during ischemia-reperfusion in rabbit.
Methods:All healthy New Zealand white rabbits were randomly assigned to six groups(n=8 each):(1) Sham-operated group(group S), rabbits were opened chest without ligating the left anterior descending coronary artery; (2) Ischemia/reperfusion group(group I/R); (3) Ischemic preconditioning group(group IPC),5min ischemia-5min reperfusion for three cycles before the long time ischemia; (4) Isoflurane group (groupⅠ), rabbits were pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout; (5) Captopril group(group C), rabbits were feeded captopril tablets (25mg·kg-1) before 24h; (6) Combination of isoflurane and captopril preconditioning group(group I+C), rabbits were feeded captopril tablets (25mg·kg-1) before 24h and pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout after 24h. After preconditioning, all rabitts were treated 30min of ischemia and 2h of reperfusion except for group S. At the end of the reperfusion, infarct size(IS) and area at risk(AAR) were accessde by Evans Blue and TTC staining. Apotosis index were detected by flow cytometry.
Results:Myocardial infarct size of group IPC, groupⅠ, group C and group I+C (33.6±3.8%,39.8±5.7%,39.6±3.4%,33.9±5.9%) were less than that of group I/R (60.7±6.0, P<0.01). Myocardial infarct size of group IPC and group I+C were less than that of groupⅠand group C (P<0.05), but distinction between group IPC and group I+C was not significantly (P>0.05). Apoptotic index of group S was the lowest in eath group (P＜0.01). Apoptotic index of group I/R was less than that of group IPC, group I, group C and group I+C(P<0.01). Apoptotic index of group I+C was less than that of groupⅠand group C, but not different with that of group IPC (P＜0.05).
Conclusions:The combination of isoflurane and captopril preconditioning can reduce myocardial infarct size and the incidence rate of apoptotic during ischemia reperfusion in rabbits. The effect was better than that of solitary preconditioning and similar with that of group IPC. The combination of isoflurane and captopril preconditioning produced a synergistic protective effect of anti-apoptosis.
Objective:To investigate the effect of the combination of isoflurane and captopril preconditioning on apoptosis-related gene and apoptosis pathway during myocardial ischemia and reperfusion in rabbit.
Methods:All healthy New Zealand white rabbits were randomly assigned to six groups (n=8 each):(1) Sham-operated group(group S), rabbits were opened chest without ligating the left anterior descending coronary artery; (2) Ischemia/reperfusion group(group I/R); (3) Ischemic preconditioning group (group IPC),5min ischemia-5min reperfusion for three cycles before the long time ischemia; (4) Isoflurane group (groupⅠ), rabbits were pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout; (5) Captopril group (group C), rabbits were feeded captopril tablets (25 mg·kg-1) before 24h; (6) Combination of isoflurane and captopril preconditioning group (group I+C), rabbits were feeded captopril tablets (25 mg·kg-1) before 24h and pretreated with 30min end-tidal 1.1% isoflurane and 15min of washout after 24h. After preconditioning, all rabitts were treated 30min of ischemia and 2h of reperfusion except for group S. At the end of the reperfusion, the heart was harvested and the activity of apoptosis-related gene (Bcl-2 and Bax) and apoptosis pathway proteins (caspase-3, caspase-8 and caspase-9) were determined by Western Blot analysis, apotosis index was detected by flow cytometry.
Results:Bcl-2/Bax ratio of group I+C and group IPC was higher than that of groupⅠand group C (P<0.01). But Bcl-2/Bax ratio of group I+C was the same high as that of group IPC. The activity of caspase-3, caspase-8 and caspase-9 of every preconditioning group were lower than that of group I/R. The activity of caspase-8 of group I+C was lower than that of other preconditioning group. The activity of caspase-9 of group IPC was lower than that of drug preconditioning group. Apotosis index of every preconditioning group was lower that of group I/R(P<0.01). Apotosis index of group I+C was lower that that of group I and group C, but ot different with that of group IPC (P>0.05).
Conclusions:The combination of isoflurane and captopril preconditioning can promote the activity of Bcl-2, inhibit the activity of Bax and increase Bcl-2/Bax ratio in myocardium during ischemia reperfusion, which maybe one of molecular mechanisms of the combina-tion of isoflurane and captopril preconditioning on cardioprotection. The combination of isoflurane and captopril preconditioning can inhibit the activity of caspase-3, caspase-8 and caspase-9 and signal transduction of apoptosis pathway, which indicate that the combination of isoflurane and captopril preconditioning can inhibit mitochondrion pathway and death receptor pathway, but mainly the latter.
引文
[1]Aronow WS. Epidemiology, Pathophysiology, Prognosis, and Treatment of Systolic and Diastolic Heart Failure. Cardiology in Review,2006,14(3):108-124.
[2]Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia:a delay of lethal cell injury in ischemia myocardium. Circulation,1986,74(5):1124-1136.
[3]Yellon DM, Baxter GF. A'second window of protection'or delayed preconditioning phenomenon:future horizons for myocardial protection? J Mol Cell Cardiol.1995,27(4):1023-1034.
[4]Bolli R. The late Phase of Preconditioning. Circ Re.2000,87(11):972-983.
[5]张红,张蓓,汤伯瑜等,一氧化氮和线粒体ATP敏感性钾通道介导血管紧张素转换酶抑制剂加强阈下预处理的作用.生理学报,2005,57(4)：453-460.
[6]Kersten JR, Schmeling TJ, Pagel PS, et al. Isoflurane mimics ischemic preconditioning via activation of K(ATP) channels:reduction of myocardial infarct size with all acute memoryphase. Anesthesiology.1997,87(2):361-370.
[7]Gumina RJ, Gross GJ. If ischemic preconditioning is the gold standard, has a platinum standard of cardioprotection arrived? Comparison with NHE inhibition. J Thromb Thrombolysis,1999,8(1):39-44.
[8]Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion:comparison、with ischemic preconditioning. Am J Physiol Heart Circ Physiol,2003,285(2):H579-588.
[9]Bolli R. The early and late phases of preconditioning against myocardial stunning and the essential role of oxyradicals in the late phase:all overview. Basic Res Cardiol,1996,91(10):57-63.
[10]Pascal C, Paul S, John G, et al. Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction in rabbits. Anesthesiology,2004,101(11):1160-1166.
[11]Degabriele NM. Griesenbach U. Sato K. et al. Critical appraisal of the mouse model of myocardial infarction. Exp physiol,2004,89(4):497-505.
[12]Kenzo yamasaki, hisayoshi fujiwara. et al. Preconditioning with15-minute ischemia extends myocardial infarct size after subsequent 30-minute ischemia in rabbits,1997,61(4):344-352.
[13]Cascio WE, Yang H, Johnson TA, et al. Electrical properties and conduction in reperfused papillary muscle. Circ Res,2001,89(9):807-814.
[14]Bolognese L, Ducci K, Angioli P, et al. Elevations in troponin I after percutaneous coronary interventions are associated with abnormal tissue level perfusion in high risk patients with non-ST-segment-elevation acute coronary syndromes. Circulation,2004,110(12):1592-1607.
[15]Belbomme D, Peynet J, Louzy M, et al. Evidence for preconditioning by isoflurane in coronary artery bypass graft surgery. Circulation,2000,101 (10): 11340-11344.
[16]Ohtake M, Morino S, Kaidoh T, et al. Three-dimensional structural changes in cerebral micro vessels after transient focal cerebral ischemia in rats:scanning electron microscopic study of corrosion casts. Neuropatheology,2004,24(3): 219-227.
[17]Zhu BQ,Sun YP, Sievers RE, et al.Comparative effects of pretreatment with captopril and iosartan on cardiovascular protection in rat model of ischemia-reperfusion, J Am Coll Cardiol,2000,35(3):787-795.
[18]Turner LA, Fujimoto K, Suzuki A, et al. The interaction of isoflurane and protein kinase C-activators on sarcolemmal KATP channels. Anesth Analg,2005, 100(6):1680-1686.
[19]Lee WH. Influence of peroxynitrite on energy metabolism and cardiac function in a rat ischemia-reperfusion model. Am J Physiol Heart Circ Physiol,2003, 285(4):H1385-1395.
[20]Lucchesi BR. Myocardial Reperfusion Injury-Role of Free Radicals and Mediators of Inflammation. San Diego, CA:Academic Press,2001,1181-1210.
[21]Liu Z, Li Z, Liu X. Effect of ginsenoside Re on cardiomyocyte apoptosis and expression of Bcl-2/Bax gene after ischemia and reperfusion in rats. J Huazhong Univ Sci Technolog Med Sci.2002,22(4):305-309.
[22]Olivetti G, Quaini F, Sala R, et al. Acute myocardial infarction in humans is associated with activation of programmed myocyte cell death in the surviving protion of the heart[J]. JMol Cell Cardiol,1996,28(9):2005-2016.
[23]Gottlieb RA, Burleson KO, Kloner RA, et al. Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest,1994,94(4):1621-1628.
[24]Saraste A, Pulkki K, Kallajoki M, et al. Apoptosis in human acute myocardial infarction. Circulation,1997,95(2):320-323.
[25]Ling H, Lou Y. Total flavones from Elsholtzia blanda reduce infarct size during acute myocardial ischemia by inhibiting myocardial apoptosis in rats. J
Ethnopharmacol,2005,101(3):169-175.
[26]Iliodromitis EK, Lazou A, Kremastinos DT. Ischemic preconditioning:protection against myocardial necrosis and apoptosis. Vase Health Risk Manag,2007,3(5): 629-637.
[27]王文亮.细胞凋亡研究进展.心脏杂志,2005,17(6)：603-606.
[28]梁绪国,潘其兴.氯沙坦与卡托普利合用对凋亡调控基因的影响.国外医学·心血管疾病分册,2003,30(2)：112-115.
[29]Thibault H, Gomez L, Donal E, et al. Acute myocardial infarction in mice: assessment of transmurality by strain rate imaging. Am J Physiol Heart Circ Physiol 2007,293(1):H496-502.
[30]Suzuki M, Sasaki N, Miki T, et al. Role of sarcolemmal K(ATP) channels in cardioprotection against ischemia/reperfusion injury in mice. J Clin Invest, 2002,109(4):509-516.
[31]Kerr J F, Wyllie AH, Currie AR. Apoptosis:a basic biological phenomenon with wide-ranging Implications In tissue kinetics. Br J Cancer,1972,26(2):239-257.
[32]Fliss H, Gatinger D. Apoptosis in ischemic and reperfused rat myocardium. Circ Res,1996,79(5):949-956.
[33]Oliveti G, Quaini F,Sala R, et al. Acute myocardial infarction in humans is as sociated with activation of programmed myocyte cell death in the surviving portion of the heart. J Mol Cell Cardiol,1996,28(9):2005-2016.
[34]Kin H, Wang NP, Mykytenko J, et al. Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-kappa B translocation and TNF alpha release.Shock,2008; 29(6): 761-768.
[35]Shirito K, Otani H, Yamamoto F, et al. MK2-/-gene knockout mouse hearts carry anti-apoptotic signal and are resistant to ischemia reperfusion injury. J Mol Cell Cardiaol,2005,38(1):93-97.
[36]Zhao ZQ, Nakamura, M, Wang NP, et al. Progressively developed myocardial apoptotic cell death during late phase of reperfusion. Apoptosis,2001,6(4): 279-290.
[37]Zaugg M, Lucchinetti E, Garcia C, et al. Anaesthetics and cardiac preconditioning. Ⅱ. Clinical implications. Br J Anaesth,2003,91(4):566-576.
[38]Davis RF, Sidi A. Effect of isflurane on the extent of myocardial necrosis and on systemic hemodynamics,regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion. Anesth Analg, 1989,69(5):575-586.
[39]Pachl J, Duska F, Waldauf P, et al. Apoptosis as an early event in the development of multiple organ failure? Physiol Res,2005,586(3):697-699.
[40]Abbate A, Salloum FN, Vecile E, et al. Anakinra a recombinant human interleukin-1 receptor antagonist, inhibits apoptosis in experimental acute myocardial infarction. Circulation,2008,117(20):2670-2683.
[41]Das A, Xi L, Kukreja RC. Phosphodiesterase-5 inhibitor sildenafil reconditions adult cardiac myocytes against necrosis and apoptosis. Essential role of nitric oxide signaling. J Biol Chem,2005,280(13):12944-12955.
[42]Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats. Lab Invest. 1996,4(1):86-107.
[43]Khoynezhad A, Jalali Z, Tortolani AJ. Apoptosis:pathophysiology and therapeutic implications for the cardiac surgeon. Ann Thorac Surg,2004,78(3): 1109-1118.
[44]Pchejetski D, Kunduzova O, Dayon A, et al. Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis. Circ Res,2007,100(1):41-49.
[45]Liang JC, Chen HR, Chiu CC, et al. Protective effect of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker, on myocardial apoptosis in ischemia-reperfusion injury. Life Sci,2006,79(13):1248-1256.
[46]Moolman JA., Hartley S, Van Wyk J, et al. Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK. Cardiovasc Drugs Ther,2006,20(1):13-25.
[47]Zhang HF, Fan Q, Qian X, et al. Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion.Apoptosis,2004,9(6):777-783.
[48]Allaouchiche B,Debon R,Goudable J,et al.Oxidative stress status duringexposure to propofol sevoflurane and desflurane.Anesthsiol Analg,2001,93(4):981-985.
[49]Tyther R, Fanning N, HalliganM, et al. The effect of the anaesthetic agent isoflurane on the rate of neutrophil apotosis in vitro. Ir JMed Sci,2001,170 (1): 41-44.
[50]Wise-Faberowski L, Raizada M K, Summners C. Oxygen and glucose deprivation-induced neuronal apoptosis is attenuated by halothane and isoflurane. Anesth Analg,2001,93 (5):1281-1287.
[51]Hou YP, Wu JL, Fan Q, et al. Plasma concentration of Fas/Fas ligand and left ventricular function in response to metoprolol in conjunction with standard treatment. Clinical Science,2006,112(5):299-304.
[52]Miyuki K, Tetsuya T, Daisuke K, et al. Effects of ACE Inhibition on Myocardial Apoptosis in an Ischemia-Reperfusion R at Heart Model. J Cardiovasc Pharmacol 2003,41(6):880-889.
[53]The Chinese Cardiac Study (CCS-1) Collaborative Group. Long-term mortality in patients with myocardial infarction:impact of early treatment with captopril for 4 weeks. Chin Med J,2001,114(2):115-118.
[54]ACE Inhibitor Myocardial Infarction Collaborative Group.Indications for ACE inhibitors in the early treatment of acute myocardial infarction:systemic overview of individual data from 100,000 patients in randomized trials. Circulation,1998,97(22):2202-2212.
[55]Ruixing Y, Dezhai Y, Jiaquan L. Effects of cardiotrophin-1 on hemodynamics and cardiomyocyte apoptosis in rats with acute myocardial infarction. J Med Invest,2004,51(1-2):29-37.
[56]Li H, Zhu H, Xu CJ, et al. Cleavage of BID by Caspase-8 mediates the mitochondrial damage in the Fas pathway of apoptesis. Cell,1998,94(4): 491-501
[57]Nishikawa S, Tatsumi T, Shiraishi J, et al. Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis. J Mol Cell Cardiol,2006,40(4):510-519.
[58]Daniel PT. Dissecting the pathways to death. Leukemia.2000,14 (12): 2035-2044.
[59]Bratton SB, Macfarlane M,Cain K,et al. Protein complexes activate distinct caspase cascades in death receptor and stress-inducced apoptosis.Exp Cell Res,2000,256(1):27-33.
[60]Schwartzman RA, Cidlowski JA. Apoptosis:the biochemistry and molecular biology of programmed cell death. Endocr Rev,1993,14(2):133-51.
[61]Reed JC. Mechanisms of apoptosis. Am J Pathol.2000,157(5):1415-1430.
[62]Chao DT, Korsmeyer SJ. BCL-2 family:regulators of cell death. Annu Rev Immunol,1998,16:395-419.
[63]Lam M, Dubyak G, ChenL,et al. Evidence that bcl-2 represses apoptosis by regulating Endoplasmic reticulnm-associates Ca2+fluxes. Proe Natl Acad Sci USA,1994,91(14):6569-6573.
[64]Tsujimoto Y, Shimizu S. The Bcl-2 family:life-or-death switch. FEBS Lett, 2000,466(1):6-10.
[65]Haunstetter A,Izumo S. Apoptosis basic mechanisms and implications for cardio va scular disease. Circulation Research,1998,82(11):1111-1129.
[66]杜敏逸,纪方,吴新民.在体外乳鼠心肌细胞缺氧的损伤及利多卡因的保护作用.中华麻醉学杂志,1999；19(3)：161-163.
[67]VanEmous JG, Nederhoff MGJ, Ruigrok TJC, et al. The role ofthe Naq channel in the accumulation of intracellular Naq during myocardial ischemia: consequences for postischemic recovery. J Mol Cell Cardiol,1997; 29(1): 85-96.
[68]Matsubara T, Ishibashi T, Nakazawa M, ct al. Effects oflidocaine on ischemic myocardial metabolism assessed by 31P-NMR in the isolated perfused rat heart. Jpn Heart J,1991; 32(4):493-504.
[69]Cheng W, Kajstura J, Nitahara JA, et al. Programmed myocyte cell death affects the viable myocardium after infarction in rats. Exp Cell Res,1996; 226(2): 316-27.
[70]Wolf BB,Green DR. Suicidal tendencies:apoptotic cell death by caspase family proteinases. J Biol Chem,1999,274(29):20049-20052.
[71]Miramar MD, Costantini P, Ravagnan L, et al. NADH oxidase activity of mitochondrial apoptosis-inducing factor. J Biol Chem,2001,276(19): 16391-16398.
[72]Zhou P,Chou J,Olea RS, et al.Solution structure of Apaf-1 CARD and its interaction with caspase-9 CARD:a structural basis for specific adaptor/caspase interaction. Proc Natl Acad Sci USA,1999,96(20):11265-11270.
[73]French LE, Tschopp J. Protein-based therapeutic approaches targeting death receptors. J Cell Death Differ,2003,10(1):117-123
[74]Wajant H, Death receptors. Essays Biochem,2003,39:53-71.
[75]Micheao O, Tschopp J, Induction If TNF receptor Ⅰ-medtiated apoptosis via two sequential signaling complexes. Cell,2003,114(2):181-190.
[76]Ashkenazi A, Dixit VM.Death receptors:signaling and modulation. Science, 1998,281(5381):1305-1380.
[77]Peter ME, Kralnmer PH. The CD95 (APO-1/Fas)DISC and beyond. Cell Death Differ,2003,10(1):26-35.
[78]Scaffidi C, Fulda S, Srinivasan A, et al. Two CD95 (APO-1/Fas) signaling pathways. EMBO,1998,17(6):1675-1687
[79]Korsmeyer SJ, Wei MC, Saito Met al. Pro-apoptotic cascade activales BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. Cell Death Differ,2000,7(12):1166-1173
[80]Li H, Zhu H, Xu CJ, et al. Cleavage ofBID by Caspase-8 mediates the mitochondrial dltlnage in the Fas pathway of apoptesis. Cell,1998,94(4): 491-501.
[81]Sun XM, Bratton SB, Butterworth M, et al. Bcl-2 and Bcl-xL inhibit CD95-mediated apoptosis by preventing mitochondrial release of Smac/DIABLO and subsequent inactivation of X-linked inhibitoe of apoptosis protein. Biol Chem,2002,277(13):11345-11351.
[82]Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci,2005,1047:248-258.
[83]Borutaite V, Jekabsone A, Morkuniene R, et al. Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction cytochrome c and apoptosis induced by heart ischemia. J Mol Cell Cardiol,2003,35(4):357-366.
[84]Eastman A, Rigas JR. Modulation of apoptosis signaling pathways and cell cycle regulation. Semin Oncol,1999,5:7-16
[85]Borutaite V, Brown, GC. Mitochondria in apoptosis of ischemic heart. FEBS Letters,2003,541(3):1-5.
[86]Maul ik N, Engelman RM, Rousou JA, et al. Ischemic preconditioning reduces apoptosis by upregulating anti-death gene Bcl-2. Circulation.1999, 100(19 Suppl):11369-75.
[87]Nakamura M, Wang NP, Zhao ZQ. et al. Preconditioning decreases Bax expression, PMN accumulation and apoptosis in reperfused rat heart. Cardiovasc Res.2000,45(3):661-70.
[88]Gill C, Mestril R, Samali A. Losing heart:the role of apoptosis in heart disease-a novel therapeutic target? FASEB J,2002,16(2):135-146.
[89]Wang C, Neff DA, Krolikowski JG, et al. The influence of B-cell lymphoma 2 protein, an antiapoptotic regulator of mitochondrial permeability transition, on isoflurane-induced and ischemic postconditioning in rabbits. Anesth Analg.2006,102(5):1355-1360.
[90]Tamba M, Torreggiani A. Free radical scavenging and copper chelation:a potentially beneficial action of captopril. Free Radic Res,2000,32(3):199-211.
[91]Zhao ZQ. Oxidative stress-elicited myocardial apoptosis during reperfusion. Curr Opin Pharmacol.2004,4(2):159-165.
[92]宋陈芳,熊世熙,尹学恩,等.几种ACEI对实验性糖尿病大鼠心肌细胞凋亡和Caspase-3及Fas、FasL基因表达影响的类效应.武汉大学学报(医学版),2008,29(1)：24-27.
[93]Odaka C, Mizuochi T.. Angiotensin-converting enzyme inhibitor captopril prevents activation-induced apoptosis by interfering with T cell activation signals. Clin Exp Immunol,2000,121(3):515-522.
[1]Ling H, Lou Y. Total flavones from Elsholtzia blanda reduce infarct size during acute myocardial ischemia by inhibiting myocardial apoptosis in rats. J Ethnopharmacol,2005,101(3):169-175.
[2]Shirito K, Otani H, Yamamoto F, et al. MK2-/-gene knockout mouse hearts carry anti-apoptotic signal and are resistant to ischemia reperfusion injury. J Mol Cell Cardiaol,2005,38(1):93-97.
[3]Schulze CJ, Wang W, Kumari R, et al Imbalance between tissue inhibitor of metallop reteinase-4 and matrixmetallop reteinases during acute myocardial correction ofmyocardial ischemia-reperfusion injury. Circulation,2003,107 (19): 2487-2492.
[4]Gottlieb, RA, Burleson, KO, Kloner, RA, et al.Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest,1994,94(4):1621-1628.
[5]Zhao ZQ, Nakamura, M, Wang NP, et al.Progressively developed myocardial apoptotic cell death during late phase of reperfusion. Apoptosis,2001,6(4): 279-290.
[6]Gill C, Mestril R, Samali A. Losing heart:the role of apoptosis in heart disease-a novel therapeutic target? FASEB J,2002,16(2):135-146.
[7]Ruixing Y, Dezhai Y, Jiaquan L. Effects of cardiotrophin-1 on hemodynamics and cardiomyocyte apoptosis in rats with acute myocardial infarction. J Med Invest, 2004,51(1-2):29-37.
[8]Sinagra G, Bussani R, Abbate A, et al. Left ventricular diastolic filling pattern at Doppler echocardiography and apoptotic rate in fatal acute myocardial infarction. Am J Cardiol,2007,99(3):307-309.
[9]Borutaite V, Brown, GC. Mitochondria in apoptosis of ischemic heart. FEBS Letters,2003,541(3):1-5.
[10]Khoynezhad A, Jalali Z, Tortolani AJ. Apoptosis:pathophysiology and therapeutic implications for the cardiac surgeon. Ann Thorac Surg,2004,78(3): 1109-1118.
[11]Matsushita K, Iwanaga S, Oda T, et al. Interleukin-6/soluble interleukin-6 receptor complex reduces infarct size via inhibiting myocardial apoptosis.Lab Invest,2005,85(10):1210-1223.
[12]Ing DJ, Zang J, Dzau VJ, et al. Modulation of cytokine-induced cardiac myocyte apoptosis by nitric oxide, Bak, and Bcl-x. Circ Res,1999,84(1):21-33.
[13]French LE, Tschopp J. Protein-based therapeutic approaches targeting death receptors. J Cell Death Differ,2003,10(1):117-123
[14]Wajant H, Death receptors. Essays Biochem,2003,39:53-71.
[15]Micheao O, Tschopp J, Induction If TNF receptor Ⅰ-medtiated apoptosis via two sequential signaling complexes. Cell,2003,114(2):181-190.
[16]Ashkenazi A, Dixit VM.Death receptors:signaling and modulation. Science, 1998,281(5381):1305-1380.
[17]Peter ME, Kralnmer PH. The CD95 (APO-1/Fas)DISC and beyond. Cell Death Differ,2003,10(1):26-35.
[18]Scaffidi C, Fulda S, Srinivasan A, et al. Two CD95 (APO-1/Fas) signaling pathways. EMBO,1998,17(6):1675-1687.
[19]Korsmeyer SJ, Wei MC, Saito Met al. Pro-apoptotic cascade activales BID, which oligomerizes BAK or BAX into pores that result in the release of cytochromec. Cell Death Differ,2000,7(12):1166-1173.
[20]Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci,2005,1047:248-258.
[21]Zhou P,Chou J,Olea RS, et al.Solution structure of Apaf-1 CARD and its interaction with caspase-9 CARD:a structural basis for specific adaptor/caspase interaction. Proc Natl Acad Sci USA,1999,96(20):11265-11270.
[21]Borutaite V, Jekabsone A, Morkuniene R, et al. Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction cytochrome c and apoptosis induced by heart ischemia. J Mol Cell Cardiol,2003,35(4):357-366.
[22]Nishikawa S, Tatsumi T, Shiraishi J, et al. Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis. J Mol Cell Cardiol,2006,40(4):510-519.
[23]Schwartzman RA, Cidlowski JA. Apoptosis:the biochemistry and molecular biology of programmed cell death. Endocr Rev,1993,14(2):133-51.
[24]Reed JC. Mechanisms of apoptosis. Am J Pathol.2000,157(5):1415-1430.
[25]Chao DT, Korsmeyer SJ. BCL-2 family:regulators of cell death. Annu Rev Immunol,1998,16:395-419.
[26]Lam M, Dubyak G, ChenL,et al. Evidence that Bcl-2 represses apoptosis by regulating Endoplasmic reticulnm-associates Ca2+ fluxes. Proe Natl Acad Sci USA,1994,91(14):6569-6573.
[27]Tsujimoto Y, Shimizu S. The Bcl-2 family:life-or-death switch. FEBS Lett, 2000,466(1):6-10.
[28]Haunstetter A,Izumo S. Apoptosis basic mechanisms and implications for cardio va scular disease. Circulation Research,1998,82(11):1111-1129.
[29]杜敏逸,纪方,吴新民.在体外乳鼠心肌细胞缺氧的损伤及利多卡因的保护作用.中华麻醉学杂志,1999,19(3)：161-163.
[30]VanEmous JG, Nederhoff MGJ, Ruigrok TJC, et al. The role ofthe Naq channel in the accumulation of intracellular Naq during myocardial ischemia: consequences for postischemic recovery. J Mol Cell Cardiol,1997,29(1):85-96.
[31]Matsubara T, Ishibashi T, Nakazawa M, ct al. Effects oflidocaine on ischemic myocardial metabolism assessed by 31P-NMR in the isolated perfused rat heart. Jpn Heart J,1991; 32(4):493-504.
[32]Nishikawa S, Tatsumi T, Shiraishi J, et al. Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis. J Mol Cell Cardiol,2006,40(4):510-519.
[33]Cheng W, Kajstura J, Nitahara JA, et al. Programmed myocyte cell death affects the viable myocardium after infarction in rats. Exp Cell Res,1996; 226(2): 316-27.
[34]Diwan A, Krenz M, Syed FM, et al. Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice. J Clin Invest,2007,117(10):2825-2833.
[35]Pchejetski D, Kunduzova O, Dayon A, et al. Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis. Circ Res,2007,100(1):41-49.
[36]Donath S, Li P, Willenbockel C, et al. Apoptosis repressor with caspase recruitment domain is required for cardioprotection in response to biomechanical and ischemic stress. Circulation,2006,113(9):1203-1212.
[37]Soeki T, Tamura Y, Shinohara H, et al. Relation between circulating soluble Fas ligand and subsequent ventricular remodelling following myocardial infarction. Heart,2003,89(3):339-341.
[38]Davis ME, Hsieh PC, Takahashi T, Tomosaburo Takahashi, et al. Local myocardial insulin-like growth factor 1 (IGF-1) delivery with biotinylated peptide nanofibers improves cell therapy for myocardial infarction. Proc Natl Acad Sci USA,2006,103(21):8155-8160.
[39]Das A, Xi L, Kukreja RC. Phosphodiesterase-5 inhibitor sildenafil preconditions adult cardiac myocytes against necrosis and apoptosis. Essential role of nitric oxide signaling. J Biol Chem,2005,280(13):12944-12955.
[40]Chen SJ, Bradley M, Lee, TC. Chemical hypoxia triggers apoptosis of cultured neonatal rat cardiac myocytes modulation by calium-regulated proteases and protein kinases. Mol Cell Bichem,1998,178(1-2):141-149.
[41]Pachl J, Duska F, Waldauf P, et al. Apoptosis as an early event in the development of multiple organ failure? Physiol Res,2005,586(3):697-699.
[42]Abbate A, Salloum FN, Vecile E, et al. Anakinra a recombinant human interleukin-1 receptor antagonist, inhibits apoptosis in experimental acute myocardial infarction. Circulation,2008,117(20):2670-2683.
[43]Moolman JA., Hartley S, Van Wyk J, et al. Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK. Cardiovasc Drugs Ther,2006,20(1):13-25.
[44]Liang JC, Chen HR, Chiu CC, et al. Protective effect of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker, on myocardial apoptosis in ischemia-reperfusion injury. Life Sci,2006,79(13):1248-1256.
[45]Zhang HF, Fan Q, Qian XX, et al. Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion.Apoptosis,2004,9(6):777-783.
[46]徐鹏霄,李全辉,徐健.卡托普利对高血压大鼠心、脑微血管内皮细胞Bax、Bcl-2表达的影响.2008,19(3)：203-205.
[47]Hou YP, Wu JL, Fan Q, et al. Plasma concentration of Fas/Fas ligand and left ventricular function in response to metoprolol in conjunction with standard treatment. Clinical Science,2006,112(5):299-304.
[48]Miyuki Kobara, Tetsuya Tatsumi, Daisuke Kambayashi et al. Effects of ACE Inh ibition on Myocardial Apoptosis in an Ischemia-ReperfusionR at Heart Model. J Cardiovasc Pharmacol 2003,41(6):880-889.
[49]李劲迈,朱清,岳欣等.卡托普利和氯沙坦对血管紧张素Ⅱ诱导血管平滑肌细胞Bcl-2和Fas基因表达的抑制作用.山东大学学报(医学版),2009,47(12)：25-29.
[50]耿召华,刘春燕,彭佑华,等.卡维地洛与培哚普利联合干预心肌梗死后心力衰竭对心肌细胞凋亡和肌浆网Ca+泵活性的影响.第四军医大学学报,2009,30(12)：1076-1079.
[51]Tamba M, Torreggiani A. Free radical scavenging and copper chelation:a potentially beneficial action of captopril. Free Radic Res,2000,32(3):199-211.
[52]宋陈芳,熊世熙,尹学恩,等.几种ACEI对实验性糖尿病大鼠心肌细胞凋亡和Caspase-3及Fas、FasL基因表达影响的类效应.武汉大学学报(医学版),2008,29(1)：24-27.
[53]麦炜颐,马莉,黄裕立,等.ACE抑制剂Ramipril对大鼠急性心肌梗死后心肌细胞凋亡和左室重构的影响.中山大学学报(医学科学版),2008,29(5)：550-555.
[54]耿召华,刘春燕,彭佑华,等.卡维地洛与培哚普利联合干预心肌梗死后心力衰竭对心肌细胞凋亡和肌浆网Ca2+泵活性的影响.第四军医大学学报,2009,30(12)：1076-1079.
[55]Dagenais GR, Pogue J, Fox K, et al. Angiotensin-converting enzyme inhibitors in stable vascular disease without left ventricular systolic dysfunction or heart failure:a combined analysis of three trials. Lancet,2006,368(9535):581-588
[56]邓昭武,任江华,宋爱华.缬沙坦和贝那普利对充血性心力衰竭患者细胞凋亡相关因子影响的比较.临床心血管病杂志,2007,23(10)：762-765.
[57]Odaka C, Mizuochi T. Angiotensin-converting enzyme inhibitor captopril prevents activation-induced apoptosis by interfering with T cell activation signals. Clin Exp Immunol,2000,121(3):515-22.
[58]Liu L, for the Chinese Cardiac Study (CCS-1) Collaborative Group. Long-term mortality in patients with myocardial infarction:impact of early treatment with captopril for 4 weeks. Chin Med J,2001,114(2):115-118.
[59]Ambrosioni E, Borghi C, Magnani B, for the Survival of Myocardial Infarction Long-term Evaluation (SMILE) study investigators. The effect of the angiotensin-converting-enzyme inhibitor zofenopril on mortality and morbidity after anterior myocardial infarction. N Engl J Med,1995,332(2):80-85.
[60]ACE Inhibitor Myocardial Infarction Collaborative Group. Indications for ACE inhibitors in the early treatment of acute myocardial infarction:systemic overview of individual data from 100,000 patients in randomized trials. Circulation,1998, 97(22):2202-2212.
[61]Ferrario CM, Strawn WB. Role of the Renin-Angiotensin-Aldosterone System and Proinflammatory Mediators in Cardiovascular Disease. Am J Cardiol,2006, 98(1):121-128.
[62]Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: results of the survival and ventricular enlargement trial. N Engl J Med,1992, 327(10):669-677.
[63]Kober L, Torp-Pedersen C, Carlsen JE, et al. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. New Engl J Med,1995, 333(25):1670-1676.
[64]Flather MD, Yusuf S, Kober L, et al. Long-term ACEI inhibitor therapy in patients with heart failure or left-ventricular dysfunction:a systemic overview of data from individual patients. Lancet,2000,355(9215):1575-1581.
[1]Malik V, Kale SC, Chowdhury UK, et al. Myocardial injury in coronary artery bypass grafting:On-pump versus off-pump comparison by measuring heart-type fatty-acid-binding protein release. Tex Heart Inst J.2006,33(3):321-327.
[2]Shim JK, Chio SH, Oh YJ, et al. The effect of mannitol on oxygenation and creatine kinase MB release in patients undergoing multivessel off-pump coronary artery bypass surgery. J Thorac Cardiovasc Surg,2007,133(3): 704-709.
[3]Kersten JR, Schmeling TJ, Pagel PS, et al. Isoflurane mimics ischemic preconditioning via activation of K(ATP)channels:reduction of myocardial infarct size with all acute memoryphase. Anesthesiology,1997,87(1):361-370.
[4]Weber NC, Schlack W. Inhalational anaesthetics and cardioprotection. Handb Exp Pharmacol.2008,182:187-207.
[5]Pascal C, Paul S, John G,et al. Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction in rabbits. Anesthesiology,2004,101(11):1160-1166.
[6]王钧,曾因明,李红.氟烷和异氟醚对缺血再灌注心肌收缩功能和ATP含量的影响.临床麻醉学杂志,1998,14(6)：335-337.
[7]李恒,杨承祥,孙凯等.挥发性麻醉药对大鼠离体心脏缺血再灌注损伤的影响. 中国病理生理杂志,2007,23(10)：891-895.
[8]Hannon JD, Cody MJ. Effects of volatile anesthetics on sarcolemmal calcium transport and sarcop lasmic reticulum calcium content in isolated myocytes. Anesthesiology,2002,96 (6):1457-1464.
[9]Lee MC, Chen CH, Kuo MC, et al. Isoflurane preconditioning induced cardio protection in patients undergoing coronary artery bypass grafting. Eur J Anaesthesiol,2006,23(10):841-847.
[10]Piriou V, Chiari P, Lhuillier F, et al. Pharmacological preconditioning: comparison of desflurane, sevoflurane, isoflurane and halothane in rabbit myocardium. Br J Anaesth,2002,89 (3):486-491.
[11]Hartley CJ, Reddy AK, Madala S, et al. Effects of isoflurane on coronary blood flow velocity in young, Old and ApoE(-/-)mice measured by doppler Ultrasound. Ultrasound Med Biol,2007,33(4):512-521.
[12]Tanaka K, Kawano T, Nakamura A, et al. Isoflurane activates sarcolemmal adenosine triphosphate-sensitive potassium channels in vascular smooth muscle cells. Anesthesiology,2007,106(5):984-991.
[13]Tsutsumi YM, Yokoyama T, Horikawa Y, et al. Reactive oxygen species trigger ischemic and pharmacological postconditioning:in vivo and in vitro characterization. Life Sci,2007,81 (15):1223-1227.
[14]张雪松,曾繁荣,左会明.乳化异氟醚预处理对缺血再灌注大鼠心肌的保护作用.中国康复理论与实践,2008,14(8)：727-728.
[15]李勇,魏继承.异氟醚心肌保护作用机制与临床应用西南军医,2009,11(4)： 737-739.
[16]Wei GZ, Zhou JJ,Wang B, et al. Diastolic Ca2+overload caused by Na+/Ca2+ exchanger during the firstminutes of reperfusion results in continued myocardial stunning. Eur J Pharmacol,2007,572 (1):1.11.
[17]Piper HM, Kasseckert SA, Schluter KD, et al. Pathophysiology of myocardial reperfusion injury. DtshMedWochenchr,2008,133 (12):586-590.
[18]Yildirim V, Doganci S, Aydin A,et al. Cardioprotective effects of sevoflurane, isoflurane, and propofol in coronary surgery patients:a randomized controlled study. Heart Surg Forum,2009,12(1):E1-9.
[19]Raphael J, Zuo Z, Abedat S,et al. isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin. Anesthesiology,2008,
108(3):415-425.
[20]An JZ, Bosnjak ZJ, Jiang MT. Myocardial protection by Isoflurane preconditioning Preserves Ca2+cycling proteins independent of sarcolemmal and mito-chondrial KATP channels.Anesth Analg,2007,105(5):1207-1213.
[21]Chen Q, Camara AK, An J, et al. Sevoflurane p reconditioning before moderated hypothermic ischemia p rotects against cytosolic [Ca2+] loading and myocardial damage in part via mitochondial KATP channels. Anesthesiology, 2002,97(4):912-920.
[22]Turner LA, Fujimoto K, Suzuki A, et al.The interaction of isoflurane and protein kinase C-activators on sarcolemmal KATP channels.Anesth Analg,2005, 100(6):1680-1686.
[23]Marinovic J, Bosnjak ZJ, Stadnicka A, et al. Preconditioning by isoflurane induces lasting sensitization of the cardiac sarcolemmal adenosine triphosphate-sensitive potassium channel by a protein kinase C-δ-mediated mechanism. Anesthesiology,2005,103(3):540-547.
[24]谭嵘,徐军美,冯华,等.异氟醚麻醉对体外循环心脏瓣膜置换术病人心肌的保护作用. 中华麻醉学杂志,2005,25(4)：316-318.
[25]曹德权,陈艳平,常业恬.异氟醚预处理对心脏瓣膜置换术病人血清一氧化氮与肌钙蛋白Ⅰ的影响. 临床麻醉学杂志,2006,22(7)：493-495.
[26]Varadarajan SG, An J, Novalija E, et al. Sevoflurane before or after ischemia improves cont ractile and metabolic function while reducing myoplasmic Ca2+ loading in intact hearts. Anesthesiology,2002,96(1):125-133.
[27]Stadnicka A, Marinovic J, Ljubkovic M, et al. Volatile anesthetic-induced cardiac preconditioning. J Anesth,2007,21(2):212-219.
[28]Patel H H, Gross E R, Peart J N, et al. Sarcolemmal KATP channel triggers delayed ischemic preconditioning in rats. Am J Physiol Heart Circ Physiol,2005, 288 (1):H445-7.
[29]Mykytenko J, Reeves J G, Kin H, et al. Persistent beneficial effect of postconditioning against infarct size:role of mitochondrial K(ATP) channels during reperfusion. B asic Res Cardiol,2008,103 (5):472-84.
[30]杨孟昌,陈玉培,张文胜,等.ATP敏感性钾通道在乳化异氟醚心肌保护效应中的作用.中国药理学通报,2009,25(2)：169-172.
[31]Krolikowski JG, BienengraeberM, et al. Inhibition of mitochondrial permeability transition enhances isoflurane2induced cardiop rotection during early reperfusion: the role of mitochondrial KATP channels. Anesth Analg,2005,101 (6) 1590-1561.
[32]Kwok WM, Martinelli AT, Fujimoto K, et al. Differentialmodulation of the cardiac adenosine tripbosphate sensitive potassimn channel by isoflurane and halothane. Anesthesiology,2002,97 (1):50-56.
[33]Sakai K, Zhang S,Ureshino H, et al. Interaction of isoflurane and cromakalim, a KATP channel opener, on coronary and systemic haemodynamics in chronically instrumented dogs. Acta Anaesthesiol Scand,2000,44 (9):1122-1127.
[34]张雷,顾尔伟,刘训芹,等.乳化异氟醚后处理对兔在体心脏缺血/再灌注损伤的保护作用.中国药理学通报,2009,25(10)：1322-1326.
[35]Raphael J, Zuo Z, Abedat S,et al.isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin. Anesthesiology, 2008; 108(3):415-425.
[36]Zhao ZQ, Corvera JS, HalkosME, et al. Inhibition of myocardial injury. by ischemic post conditioning during reperfusion:Comparison with ischemic p recond itioning. Am J Circ Physiol,2003,285(2):H579-H588.
[37]Belbomme D,Peynet J,Louzy M,David HM. Evidence for preconditioning by isoflurane in coronary artery bypass graft surgery. Circulation,2000,101(10)：11340-11344.
[38]RAN ke, DUAN Kai-ming, ZOU Ding-quan, et al. Protective effects of isoflurane delayed preconditioning on rabbit myocardium after ischemic-reperfusion. CLINICAL MEDICINE,2007,27 (10):69-72.
[39]张明香,刘尚国.异氟醚在非体外循环冠状动脉搭桥术中心肌保护作用的临床研究.中国煤炭工业医学杂志,2005,8(8)：892-893.
[40]Hein M, Roehl AB, Baumert JH, et al. Establishment of a porcine right ventricular infarction model for cardioprotective actions of xenon and isoflurane. Acta Anaesthesiol Scand.2008;52(9):1194-1203.
[41]Weber NC, Kandker JC, Schlack W, et al. Intermitted pharmacologic pretreatment by xenon, isoflurane, nitrous oxide, and the opioid morphine prevents tumor necrosis factor alphainduced adhesion molecule expression in human umbilical vein endothelial cells. Anesthesiology,2008,108(2):199-207.
[42]Wippermann J, Albes JM, Hartrumpf, et al. Comparison of minimally invasive closed circuit extracorporeal circulation with conventional
cardiopulmonary bypass and with off-pump technique in CABG patients: selected parameters of coagulation and inflammatory system. Eur J Cardiothorac Surg,2005,28(1):127-132[43]胡国昌,曾因明.异氟醚抑制冠状循环的中性粒细胞-内皮细胞相互作用.Anesthesia and Analgesia,2002,94 (8):49-56.
[44]阮文燕,徐军美,金丽艳,等.异氟醚预处理对心脏瓣膜置换术病人血肌红蛋白、vWF和心肌细胞显微结构的影响.中国新药与临床杂志,2009,28(11)：819-824.
[45]Harada N,Miura T,Dairaku Y, et al. NO donor-activated PKC-8 plays a pivotal role in ischemic myocardial protection through accelerated opening of mitochondrial K-ATP channels. J Cardiovasc Pharmacol,2004,44 (1):35-41
[46]Kuno A, Critz SD, Cohen MV, et al. Nicorandil opens mitochondrial K (ATP)channels not only directly but also through a NO-PKG-dependent pathway.Basic Res Cardiol,2007,102 (1):73-79.
[47]李进,袁世荧,丰新民.诱导型一氧化氮合酶在异氟醚延迟相预处理心肌保护中的作用.临床麻醉学杂志,2008,24(10)：676-678.
[48]曹德权,陈艳平,常业恬.异氟醚预处理对心脏瓣膜置换术病人血清一氧化氮与肌钙蛋白Ⅰ的影响.临床麻醉学杂志,2006,22(7)：493-495.
[49]Pravdic D, Sedlic F, Mio Y, et al. Anesthetic-induced preconditioning delays opening of mitochondrial permeability transition pore via protein Kinase C-epsilon-mediated pathway. Anesthesiology.2009,111 (2):267-74.
[50]Krolikowski JG, Weihrauch D, Bienengraeber M et al. Role of Erkl/2, p70s6K, and eNOS in isoflurane-induced cardioprotection during early reperfusion in vivo. Can J Anaesth,2006,53(2):174-182.
[51]Newberg LA, Michenfelder JD. Cerebral protection by isoflurane during hypoxemia or ischemia. Anesthesiology,1983,59(1):29-35.
[52]Hanouz JL, Yvon A, MassettiM, et al. Mechanisms of desflurane-induced p reconditioning in isolated human right atria in vitro. Anesthesiology,2002,97 (1):33-41.
[53]Tas PW, Eisemann C, Roewer N. The volatile anesthetic isoflurane suppresses spontaneous calcium oscillations in vitro in rat hippocampal neurons by activation of adenosine Al receptors. Neurosci Lett,2003,338 (3):229-232.
[54]Zheng S, Zuo Z. Isoflurane preconditioning decreases glutamate receptor overactivation-induced Purkinje neuronal injury in rat cerebellar slices.Brain Res, 2005,1054 (2):143-151.
[55]MoeMC, Berg JJ, Larsen GA, et al. The effect of isoflurane and sevoflurane on cerebrocortical presynaptic Ca2+and protein kinase C activity. NeurosurgAnesthediol,2003,15 (3):209-214.
[56]Kapinya KJ, Lowl D, Futterer C, et al. Tolerance against ischemic neuronal injury can be induced by volatile anesthetics and is inducible NO synthase dependent.Stroke,2002,33 (7):1889-1898.
[57]Xiong L Z, Zheng Y,Wu BI, et al. Preconditioning with Isoflurane Produces Dose-Dependent Neuroprotection via Activation of Adenosine Triphosphate-Regulated Potassium Channels After Focal Cerebral Ischemia in Rats. Aneath Analg,2003,96(1):233-237.
[58]李继庆,张联峰,王洋松,等.异氟醚预处理对大鼠全脑缺血再灌注损伤的保护作用.中华麻醉学杂志,2003,20(7)：515-517.
[59]吴春明,熊利泽,朱正华,等.异氟醚预处理脑保护作用的剂量-效应关系.第四军医大学学报,2002,23(15)：1357-1359.
[60]王胜,王志萍,张兆航,等.异氟醚预处理通过激活MAPK信号通路产生对离体大鼠脑的神经保护作用.国际麻醉学与复苏杂志,2006,27(2)：88-91.
[61]Engelhard K, Werner C, Reeker W, et al. Desflurane and isoflurane improve neurological outcome after incomplete cerebral ischemia in rats. Br J Anaesth, 1999,83(3):415-421.
[62]吴明春,熊利泽,朱正华,等.异氟醚预处理脑保护作用的剂量-效应关系.第四军医大学学报,2002,23(15)：1357-1359.
[63]刘艳红,熊利泽,陈绍洋,等.钠离子通道在异氟醚预处理诱导的脑保护中的作用.第四军医大学学报,2002,23(15)：1366-1368.
[64]刘艳红,熊利泽,王强,等.异氟醚预处理对大鼠脑缺血/再灌注损伤细胞内游离钙的影响.中国临床药理学与治疗学,2005,10(8)：909-912.
[65]Kudo M, Aono M, Lee Y, et al. Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures. Anesthesiology, 2001,94(2):303-312.
[66]段开明,欧阳文,夏月峰,等.异氟醚麻醉对大鼠海马蛋白质组的影响.临床麻醉学杂志,2008,24(3)：239-241.
[67]Sullivan BL,Leu D, Taylor DM, et al. Isoflurane prevents delayed cell death in an organotypic slice culture model cerebral ischemia. Anesthesiology,2002,96 (1):189-195.
[68]沈洁,陈卫民.一氧化氮在异氟烷预处理脑保护中的作用.中国现代医学杂志,2007,17(21).2593-2596.
[69]Ito T, Deng X, Carr B, et al. Bel-2 phosphorylation required for anti-apoptosis function. J Biol Chem,1997,272 (18):11671-11673.
[70]孙永海,岳云,王云.再灌注期吸入异氟醚对不同程度大鼠脑缺血再灌注损伤的影响.中华麻醉学杂志.2004,24(12)：901-904.
[71]邵建林,朱俊超,吴滨阳,等.异氟醚、七氟醚和地氟醚预处理对脑缺血再灌注损伤大鼠海马CBS/H2S、iNOS/NO和HO-1/CO的影响.中华麻醉学杂志,2006,26(6)：907-910.
[72]Sullivan B L, Leu D, Taylor D M, et al. Isoflurane prevents delayed cell death in an organotypic slice culture model of cerebral ischemia. Anesthesiology,2002, 96(1):189-195.
[73]沈洁,吴兴茂,陈卫民.异氟烷预处理对缺血再灌注损伤鼠脑组织中Bcl-2和Bax的mRNA表达的影响.中国医科大学学报,2007,6(2)：138-140.
[74]李继庆,李志学,张联峰,等.异氟烷预处理对大鼠全脑缺血再灌注损伤保护机制的研究.哈尔滨医科大学学报,2004,38(6)：522-525.
[75]Johnson GL, Lapadat R. Mitogen-activated protein kinase pathwaysmediated by ERK, JNK, and p38 protein kinases. Science,2002,298 (1):1911-1912.
[76]Zheng S, Zuo Z. Isoflurane Preconditioning Induces Neuroprotection against Ischemia via Activation of P38 Mitogen-Activated Protein Kinases.Mol Pharmacol,2004,65 (5):1172-1180.
[77]Wise-Faberowski L, Pearlstein RD, Warner DS.NMDA-induced apoptosis in mixed neuronal/glial cortical cell cultures:the effects of isoflurane and dizocilpine. Neurosurg Anesthesiol,2006,18(4):240-246.
[78]黄戈.体外循环与肺保护.医学研究生报,2004,17(3)：2732-2751.
[79]陈艳平,曹德权,常业恬.异氟醚对家兔肺缺血再灌注损伤的影响.中华麻醉学杂志,2001,8(21)：483-486.
[80]王婷,蒋豪,薛张纲,等.异氟醚对大鼠肺缺血-再灌注损伤的影响.临床麻醉学杂志,2005,21(10)：713-715.
[81]王井,蒋豪,薛张纲,等.异氟醚对大鼠肺缺血再灌注损伤的保护作用.中华麻醉学杂志,2006,26(2)：140-143.
[82]王婷,蒋豪,薛张纲,等.异氟醚对大鼠肺缺血再灌注损伤时NF-κB及中性粒细胞趋化因子表达的影响.复旦学报(医学版),2005,32(4)：394-400.
[83]赵黎丽,徐道妙,覃军.异氟醚预处理对犬体外循环肺损伤的保护作用.中南 大学学报(医学版)2005,30(5)：620-621.
[84]Reutershan J, Chang D, Hayes JK, et al. Protective effects of isoflurane p retreatment in endotoxin induced lung injury. Anesthesiology,2006,104(3): 511-517.
[85]Giraud O,Molliex S, Rolland C, et al. Halogenated anesthetics reduce interleukin-1 [beta]-induced cytokine secretion by rat alveolar type II cells in primary culture. Anesthesiology,2003,98 (1):74-81.
[86]安海燕,杨拔贤.不同浓度异氟烷吸入对大鼠炎症反应的影响.山东医药,2009,49(11)：24-26.
[87]徐道妙,郭曲练,申建初,等犬单肺移植后肺动脉高压与血浆TXA2代谢的关系.中华麻醉学杂志,1998,18(3)：179-180.
[88]上官王宁,刘进.挥发性吸入麻醉药对肺的作用.国际麻醉学与复苏杂志,2007,28(4)：320-322.
[89]张健,叶敏,彭章龙,等.安氟醚和异氟醚对肝脏缺血再灌注损害的影响.中华麻醉学杂志,2000,20(4)：223-225.
[90]Morioka D, Kubota T, Sekido H, et al. Prostaglandin El improved the function of transplanted fatty liver in a rat reduced-size-liver transplantation model under conditions of permissible cold preservation. Liver Transpl,2003,9(1):79-86.
[91]王旭东,卢雅立,王飞,等.七氟烷和异氟烷对肝脏缺血再灌注损伤的影响.中山大学学报(医学科学版),2008,29(1)：30-33.
[92]Shah V, Kamath PS. Nitric oxide in liver transplantation:Pathobiology and clinical implications. Liver Transpl,2003,9(1):1-11.
[93]李泉,俞卫锋,徐学武,等.异氟醚减少离体鼠肝缺氧-复氧损伤.临床麻醉学杂志,2005,21(9)：618-620.
[94]徐广民,陶国才,易斌.异氟烷对大鼠肝脏缺血再灌注损伤时细胞间黏附分子-1表达的影响.第三军医大学学报,2008,30(3)：241-243.
[95]俞卫锋,李丽,徐学武,等.异氟烷改善离体鼠肝缺氧-复氧后氧供耗平衡.第二军医大学学报,2006,27(2)：200-202.
[96]Krumschnabel G, Manzl C, Schwarzbaum PJ. Importance of glycolysis for t he energetics of anoxia-tolerant and anoxia-intolerant teleost hepatocytes. Physiol Biochem Zool,2001,74:413-419.
[97]俞卫锋,李泉,曹云飞,等.异氟烷保护缺氧肝细胞的能量平衡.第二军医大学学报,2002,23(6)：614-616.
[98]郁勤燕,王祥瑞,杭燕南,等.地氟醚、七氟醚和异氟醚对猪肝血流及肝氧 供需平衡的影响.中华麻醉学杂志,2000,20(10)：624-627.
[99]李泉,俞卫锋,曹云飞,等.异氟醚对缺氧或复氧肝细胞能量平衡的保护作用.临床麻醉学杂志,2005,21(4)：257-259.
[100]李爱芝,马加海.吸入麻醉对大鼠急性肾缺血再灌注损伤的保护.医学动物防治,2009,25(4)：262-266.
[101]Lee H T, Ota-Setlik A, Fu Y, et al. Differential protective effects of volatile anesthetics against renal ischemia-reperfusion injury in vivo. Anesthesiology, 2004,101(6):1313-1324.
[2]Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia:a delay of lethal cell injury in ischemia myocardium. Circulation,1986,74(5):1124-1136.
[3]Yellon DM, Baxter GF. A'second window of protection'or delayed preconditioning phenomenon:future horizons for myocardial protection? J Mol Cell Cardiol.1995,27(4):1023-1034.
[4]Bolli R. The late Phase of Preconditioning. Circ Re.2000,87(11):972-983.
[5]张红,张蓓,汤伯瑜等,一氧化氮和线粒体ATP敏感性钾通道介导血管紧张素转换酶抑制剂加强阈下预处理的作用.生理学报,2005,57(4)：453-460.
[6]Kersten JR, Schmeling TJ, Pagel PS, et al. Isoflurane mimics ischemic preconditioning via activation of K(ATP) channels:reduction of myocardial infarct size with all acute memoryphase. Anesthesiology.1997,87(2):361-370.
[7]Gumina RJ, Gross GJ. If ischemic preconditioning is the gold standard, has a platinum standard of cardioprotection arrived? Comparison with NHE inhibition. J Thromb Thrombolysis,1999,8(1):39-44.
[8]Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion:comparison、with ischemic preconditioning. Am J Physiol Heart Circ Physiol,2003,285(2):H579-588.
[9]Bolli R. The early and late phases of preconditioning against myocardial stunning and the essential role of oxyradicals in the late phase:all overview. Basic Res Cardiol,1996,91(10):57-63.
[10]Pascal C, Paul S, John G, et al. Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction in rabbits. Anesthesiology,2004,101(11):1160-1166.
[11]Degabriele NM. Griesenbach U. Sato K. et al. Critical appraisal of the mouse model of myocardial infarction. Exp physiol,2004,89(4):497-505.
[12]Kenzo yamasaki, hisayoshi fujiwara. et al. Preconditioning with15-minute ischemia extends myocardial infarct size after subsequent 30-minute ischemia in rabbits,1997,61(4):344-352.
[13]Cascio WE, Yang H, Johnson TA, et al. Electrical properties and conduction in reperfused papillary muscle. Circ Res,2001,89(9):807-814.
[14]Bolognese L, Ducci K, Angioli P, et al. Elevations in troponin I after percutaneous coronary interventions are associated with abnormal tissue level perfusion in high risk patients with non-ST-segment-elevation acute coronary syndromes. Circulation,2004,110(12):1592-1607.
[15]Belbomme D, Peynet J, Louzy M, et al. Evidence for preconditioning by isoflurane in coronary artery bypass graft surgery. Circulation,2000,101 (10): 11340-11344.
[16]Ohtake M, Morino S, Kaidoh T, et al. Three-dimensional structural changes in cerebral micro vessels after transient focal cerebral ischemia in rats:scanning electron microscopic study of corrosion casts. Neuropatheology,2004,24(3): 219-227.
[17]Zhu BQ,Sun YP, Sievers RE, et al.Comparative effects of pretreatment with captopril and iosartan on cardiovascular protection in rat model of ischemia-reperfusion, J Am Coll Cardiol,2000,35(3):787-795.
[18]Turner LA, Fujimoto K, Suzuki A, et al. The interaction of isoflurane and protein kinase C-activators on sarcolemmal KATP channels. Anesth Analg,2005, 100(6):1680-1686.
[19]Lee WH. Influence of peroxynitrite on energy metabolism and cardiac function in a rat ischemia-reperfusion model. Am J Physiol Heart Circ Physiol,2003, 285(4):H1385-1395.
[20]Lucchesi BR. Myocardial Reperfusion Injury-Role of Free Radicals and Mediators of Inflammation. San Diego, CA:Academic Press,2001,1181-1210.
[21]Liu Z, Li Z, Liu X. Effect of ginsenoside Re on cardiomyocyte apoptosis and expression of Bcl-2/Bax gene after ischemia and reperfusion in rats. J Huazhong Univ Sci Technolog Med Sci.2002,22(4):305-309.
[22]Olivetti G, Quaini F, Sala R, et al. Acute myocardial infarction in humans is associated with activation of programmed myocyte cell death in the surviving protion of the heart[J]. JMol Cell Cardiol,1996,28(9):2005-2016.
[23]Gottlieb RA, Burleson KO, Kloner RA, et al. Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest,1994,94(4):1621-1628.
[24]Saraste A, Pulkki K, Kallajoki M, et al. Apoptosis in human acute myocardial infarction. Circulation,1997,95(2):320-323.
[25]Ling H, Lou Y. Total flavones from Elsholtzia blanda reduce infarct size during acute myocardial ischemia by inhibiting myocardial apoptosis in rats. J
Ethnopharmacol,2005,101(3):169-175.
[26]Iliodromitis EK, Lazou A, Kremastinos DT. Ischemic preconditioning:protection against myocardial necrosis and apoptosis. Vase Health Risk Manag,2007,3(5): 629-637.
[27]王文亮.细胞凋亡研究进展.心脏杂志,2005,17(6)：603-606.
[28]梁绪国,潘其兴.氯沙坦与卡托普利合用对凋亡调控基因的影响.国外医学·心血管疾病分册,2003,30(2)：112-115.
[29]Thibault H, Gomez L, Donal E, et al. Acute myocardial infarction in mice: assessment of transmurality by strain rate imaging. Am J Physiol Heart Circ Physiol 2007,293(1):H496-502.
[30]Suzuki M, Sasaki N, Miki T, et al. Role of sarcolemmal K(ATP) channels in cardioprotection against ischemia/reperfusion injury in mice. J Clin Invest, 2002,109(4):509-516.
[31]Kerr J F, Wyllie AH, Currie AR. Apoptosis:a basic biological phenomenon with wide-ranging Implications In tissue kinetics. Br J Cancer,1972,26(2):239-257.
[32]Fliss H, Gatinger D. Apoptosis in ischemic and reperfused rat myocardium. Circ Res,1996,79(5):949-956.
[33]Oliveti G, Quaini F,Sala R, et al. Acute myocardial infarction in humans is as sociated with activation of programmed myocyte cell death in the surviving portion of the heart. J Mol Cell Cardiol,1996,28(9):2005-2016.
[34]Kin H, Wang NP, Mykytenko J, et al. Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-kappa B translocation and TNF alpha release.Shock,2008; 29(6): 761-768.
[35]Shirito K, Otani H, Yamamoto F, et al. MK2-/-gene knockout mouse hearts carry anti-apoptotic signal and are resistant to ischemia reperfusion injury. J Mol Cell Cardiaol,2005,38(1):93-97.
[36]Zhao ZQ, Nakamura, M, Wang NP, et al. Progressively developed myocardial apoptotic cell death during late phase of reperfusion. Apoptosis,2001,6(4): 279-290.
[37]Zaugg M, Lucchinetti E, Garcia C, et al. Anaesthetics and cardiac preconditioning. Ⅱ. Clinical implications. Br J Anaesth,2003,91(4):566-576.
[38]Davis RF, Sidi A. Effect of isflurane on the extent of myocardial necrosis and on systemic hemodynamics,regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion. Anesth Analg, 1989,69(5):575-586.
[39]Pachl J, Duska F, Waldauf P, et al. Apoptosis as an early event in the development of multiple organ failure? Physiol Res,2005,586(3):697-699.
[40]Abbate A, Salloum FN, Vecile E, et al. Anakinra a recombinant human interleukin-1 receptor antagonist, inhibits apoptosis in experimental acute myocardial infarction. Circulation,2008,117(20):2670-2683.
[41]Das A, Xi L, Kukreja RC. Phosphodiesterase-5 inhibitor sildenafil reconditions adult cardiac myocytes against necrosis and apoptosis. Essential role of nitric oxide signaling. J Biol Chem,2005,280(13):12944-12955.
[42]Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats. Lab Invest. 1996,4(1):86-107.
[43]Khoynezhad A, Jalali Z, Tortolani AJ. Apoptosis:pathophysiology and therapeutic implications for the cardiac surgeon. Ann Thorac Surg,2004,78(3): 1109-1118.
[44]Pchejetski D, Kunduzova O, Dayon A, et al. Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis. Circ Res,2007,100(1):41-49.
[45]Liang JC, Chen HR, Chiu CC, et al. Protective effect of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker, on myocardial apoptosis in ischemia-reperfusion injury. Life Sci,2006,79(13):1248-1256.
[46]Moolman JA., Hartley S, Van Wyk J, et al. Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK. Cardiovasc Drugs Ther,2006,20(1):13-25.
[47]Zhang HF, Fan Q, Qian X, et al. Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion.Apoptosis,2004,9(6):777-783.
[48]Allaouchiche B,Debon R,Goudable J,et al.Oxidative stress status duringexposure to propofol sevoflurane and desflurane.Anesthsiol Analg,2001,93(4):981-985.
[49]Tyther R, Fanning N, HalliganM, et al. The effect of the anaesthetic agent isoflurane on the rate of neutrophil apotosis in vitro. Ir JMed Sci,2001,170 (1): 41-44.
[50]Wise-Faberowski L, Raizada M K, Summners C. Oxygen and glucose deprivation-induced neuronal apoptosis is attenuated by halothane and isoflurane. Anesth Analg,2001,93 (5):1281-1287.
[51]Hou YP, Wu JL, Fan Q, et al. Plasma concentration of Fas/Fas ligand and left ventricular function in response to metoprolol in conjunction with standard treatment. Clinical Science,2006,112(5):299-304.
[52]Miyuki K, Tetsuya T, Daisuke K, et al. Effects of ACE Inhibition on Myocardial Apoptosis in an Ischemia-Reperfusion R at Heart Model. J Cardiovasc Pharmacol 2003,41(6):880-889.
[53]The Chinese Cardiac Study (CCS-1) Collaborative Group. Long-term mortality in patients with myocardial infarction:impact of early treatment with captopril for 4 weeks. Chin Med J,2001,114(2):115-118.
[54]ACE Inhibitor Myocardial Infarction Collaborative Group.Indications for ACE inhibitors in the early treatment of acute myocardial infarction:systemic overview of individual data from 100,000 patients in randomized trials. Circulation,1998,97(22):2202-2212.
[55]Ruixing Y, Dezhai Y, Jiaquan L. Effects of cardiotrophin-1 on hemodynamics and cardiomyocyte apoptosis in rats with acute myocardial infarction. J Med Invest,2004,51(1-2):29-37.
[56]Li H, Zhu H, Xu CJ, et al. Cleavage of BID by Caspase-8 mediates the mitochondrial damage in the Fas pathway of apoptesis. Cell,1998,94(4): 491-501
[57]Nishikawa S, Tatsumi T, Shiraishi J, et al. Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis. J Mol Cell Cardiol,2006,40(4):510-519.
[58]Daniel PT. Dissecting the pathways to death. Leukemia.2000,14 (12): 2035-2044.
[59]Bratton SB, Macfarlane M,Cain K,et al. Protein complexes activate distinct caspase cascades in death receptor and stress-inducced apoptosis.Exp Cell Res,2000,256(1):27-33.
[60]Schwartzman RA, Cidlowski JA. Apoptosis:the biochemistry and molecular biology of programmed cell death. Endocr Rev,1993,14(2):133-51.
[61]Reed JC. Mechanisms of apoptosis. Am J Pathol.2000,157(5):1415-1430.
[62]Chao DT, Korsmeyer SJ. BCL-2 family:regulators of cell death. Annu Rev Immunol,1998,16:395-419.
[63]Lam M, Dubyak G, ChenL,et al. Evidence that bcl-2 represses apoptosis by regulating Endoplasmic reticulnm-associates Ca2+fluxes. Proe Natl Acad Sci USA,1994,91(14):6569-6573.
[64]Tsujimoto Y, Shimizu S. The Bcl-2 family:life-or-death switch. FEBS Lett, 2000,466(1):6-10.
[65]Haunstetter A,Izumo S. Apoptosis basic mechanisms and implications for cardio va scular disease. Circulation Research,1998,82(11):1111-1129.
[66]杜敏逸,纪方,吴新民.在体外乳鼠心肌细胞缺氧的损伤及利多卡因的保护作用.中华麻醉学杂志,1999；19(3)：161-163.
[67]VanEmous JG, Nederhoff MGJ, Ruigrok TJC, et al. The role ofthe Naq channel in the accumulation of intracellular Naq during myocardial ischemia: consequences for postischemic recovery. J Mol Cell Cardiol,1997; 29(1): 85-96.
[68]Matsubara T, Ishibashi T, Nakazawa M, ct al. Effects oflidocaine on ischemic myocardial metabolism assessed by 31P-NMR in the isolated perfused rat heart. Jpn Heart J,1991; 32(4):493-504.
[69]Cheng W, Kajstura J, Nitahara JA, et al. Programmed myocyte cell death affects the viable myocardium after infarction in rats. Exp Cell Res,1996; 226(2): 316-27.
[70]Wolf BB,Green DR. Suicidal tendencies:apoptotic cell death by caspase family proteinases. J Biol Chem,1999,274(29):20049-20052.
[71]Miramar MD, Costantini P, Ravagnan L, et al. NADH oxidase activity of mitochondrial apoptosis-inducing factor. J Biol Chem,2001,276(19): 16391-16398.
[72]Zhou P,Chou J,Olea RS, et al.Solution structure of Apaf-1 CARD and its interaction with caspase-9 CARD:a structural basis for specific adaptor/caspase interaction. Proc Natl Acad Sci USA,1999,96(20):11265-11270.
[73]French LE, Tschopp J. Protein-based therapeutic approaches targeting death receptors. J Cell Death Differ,2003,10(1):117-123
[74]Wajant H, Death receptors. Essays Biochem,2003,39:53-71.
[75]Micheao O, Tschopp J, Induction If TNF receptor Ⅰ-medtiated apoptosis via two sequential signaling complexes. Cell,2003,114(2):181-190.
[76]Ashkenazi A, Dixit VM.Death receptors:signaling and modulation. Science, 1998,281(5381):1305-1380.
[77]Peter ME, Kralnmer PH. The CD95 (APO-1/Fas)DISC and beyond. Cell Death Differ,2003,10(1):26-35.
[78]Scaffidi C, Fulda S, Srinivasan A, et al. Two CD95 (APO-1/Fas) signaling pathways. EMBO,1998,17(6):1675-1687
[79]Korsmeyer SJ, Wei MC, Saito Met al. Pro-apoptotic cascade activales BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. Cell Death Differ,2000,7(12):1166-1173
[80]Li H, Zhu H, Xu CJ, et al. Cleavage ofBID by Caspase-8 mediates the mitochondrial dltlnage in the Fas pathway of apoptesis. Cell,1998,94(4): 491-501.
[81]Sun XM, Bratton SB, Butterworth M, et al. Bcl-2 and Bcl-xL inhibit CD95-mediated apoptosis by preventing mitochondrial release of Smac/DIABLO and subsequent inactivation of X-linked inhibitoe of apoptosis protein. Biol Chem,2002,277(13):11345-11351.
[82]Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci,2005,1047:248-258.
[83]Borutaite V, Jekabsone A, Morkuniene R, et al. Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction cytochrome c and apoptosis induced by heart ischemia. J Mol Cell Cardiol,2003,35(4):357-366.
[84]Eastman A, Rigas JR. Modulation of apoptosis signaling pathways and cell cycle regulation. Semin Oncol,1999,5:7-16
[85]Borutaite V, Brown, GC. Mitochondria in apoptosis of ischemic heart. FEBS Letters,2003,541(3):1-5.
[86]Maul ik N, Engelman RM, Rousou JA, et al. Ischemic preconditioning reduces apoptosis by upregulating anti-death gene Bcl-2. Circulation.1999, 100(19 Suppl):11369-75.
[87]Nakamura M, Wang NP, Zhao ZQ. et al. Preconditioning decreases Bax expression, PMN accumulation and apoptosis in reperfused rat heart. Cardiovasc Res.2000,45(3):661-70.
[88]Gill C, Mestril R, Samali A. Losing heart:the role of apoptosis in heart disease-a novel therapeutic target? FASEB J,2002,16(2):135-146.
[89]Wang C, Neff DA, Krolikowski JG, et al. The influence of B-cell lymphoma 2 protein, an antiapoptotic regulator of mitochondrial permeability transition, on isoflurane-induced and ischemic postconditioning in rabbits. Anesth Analg.2006,102(5):1355-1360.
[90]Tamba M, Torreggiani A. Free radical scavenging and copper chelation:a potentially beneficial action of captopril. Free Radic Res,2000,32(3):199-211.
[91]Zhao ZQ. Oxidative stress-elicited myocardial apoptosis during reperfusion. Curr Opin Pharmacol.2004,4(2):159-165.
[92]宋陈芳,熊世熙,尹学恩,等.几种ACEI对实验性糖尿病大鼠心肌细胞凋亡和Caspase-3及Fas、FasL基因表达影响的类效应.武汉大学学报(医学版),2008,29(1)：24-27.
[93]Odaka C, Mizuochi T.. Angiotensin-converting enzyme inhibitor captopril prevents activation-induced apoptosis by interfering with T cell activation signals. Clin Exp Immunol,2000,121(3):515-522.
[1]Ling H, Lou Y. Total flavones from Elsholtzia blanda reduce infarct size during acute myocardial ischemia by inhibiting myocardial apoptosis in rats. J Ethnopharmacol,2005,101(3):169-175.
[2]Shirito K, Otani H, Yamamoto F, et al. MK2-/-gene knockout mouse hearts carry anti-apoptotic signal and are resistant to ischemia reperfusion injury. J Mol Cell Cardiaol,2005,38(1):93-97.
[3]Schulze CJ, Wang W, Kumari R, et al Imbalance between tissue inhibitor of metallop reteinase-4 and matrixmetallop reteinases during acute myocardial correction ofmyocardial ischemia-reperfusion injury. Circulation,2003,107 (19): 2487-2492.
[4]Gottlieb, RA, Burleson, KO, Kloner, RA, et al.Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest,1994,94(4):1621-1628.
[5]Zhao ZQ, Nakamura, M, Wang NP, et al.Progressively developed myocardial apoptotic cell death during late phase of reperfusion. Apoptosis,2001,6(4): 279-290.
[6]Gill C, Mestril R, Samali A. Losing heart:the role of apoptosis in heart disease-a novel therapeutic target? FASEB J,2002,16(2):135-146.
[7]Ruixing Y, Dezhai Y, Jiaquan L. Effects of cardiotrophin-1 on hemodynamics and cardiomyocyte apoptosis in rats with acute myocardial infarction. J Med Invest, 2004,51(1-2):29-37.
[8]Sinagra G, Bussani R, Abbate A, et al. Left ventricular diastolic filling pattern at Doppler echocardiography and apoptotic rate in fatal acute myocardial infarction. Am J Cardiol,2007,99(3):307-309.
[9]Borutaite V, Brown, GC. Mitochondria in apoptosis of ischemic heart. FEBS Letters,2003,541(3):1-5.
[10]Khoynezhad A, Jalali Z, Tortolani AJ. Apoptosis:pathophysiology and therapeutic implications for the cardiac surgeon. Ann Thorac Surg,2004,78(3): 1109-1118.
[11]Matsushita K, Iwanaga S, Oda T, et al. Interleukin-6/soluble interleukin-6 receptor complex reduces infarct size via inhibiting myocardial apoptosis.Lab Invest,2005,85(10):1210-1223.
[12]Ing DJ, Zang J, Dzau VJ, et al. Modulation of cytokine-induced cardiac myocyte apoptosis by nitric oxide, Bak, and Bcl-x. Circ Res,1999,84(1):21-33.
[13]French LE, Tschopp J. Protein-based therapeutic approaches targeting death receptors. J Cell Death Differ,2003,10(1):117-123
[14]Wajant H, Death receptors. Essays Biochem,2003,39:53-71.
[15]Micheao O, Tschopp J, Induction If TNF receptor Ⅰ-medtiated apoptosis via two sequential signaling complexes. Cell,2003,114(2):181-190.
[16]Ashkenazi A, Dixit VM.Death receptors:signaling and modulation. Science, 1998,281(5381):1305-1380.
[17]Peter ME, Kralnmer PH. The CD95 (APO-1/Fas)DISC and beyond. Cell Death Differ,2003,10(1):26-35.
[18]Scaffidi C, Fulda S, Srinivasan A, et al. Two CD95 (APO-1/Fas) signaling pathways. EMBO,1998,17(6):1675-1687.
[19]Korsmeyer SJ, Wei MC, Saito Met al. Pro-apoptotic cascade activales BID, which oligomerizes BAK or BAX into pores that result in the release of cytochromec. Cell Death Differ,2000,7(12):1166-1173.
[20]Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci,2005,1047:248-258.
[21]Zhou P,Chou J,Olea RS, et al.Solution structure of Apaf-1 CARD and its interaction with caspase-9 CARD:a structural basis for specific adaptor/caspase interaction. Proc Natl Acad Sci USA,1999,96(20):11265-11270.
[21]Borutaite V, Jekabsone A, Morkuniene R, et al. Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction cytochrome c and apoptosis induced by heart ischemia. J Mol Cell Cardiol,2003,35(4):357-366.
[22]Nishikawa S, Tatsumi T, Shiraishi J, et al. Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis. J Mol Cell Cardiol,2006,40(4):510-519.
[23]Schwartzman RA, Cidlowski JA. Apoptosis:the biochemistry and molecular biology of programmed cell death. Endocr Rev,1993,14(2):133-51.
[24]Reed JC. Mechanisms of apoptosis. Am J Pathol.2000,157(5):1415-1430.
[25]Chao DT, Korsmeyer SJ. BCL-2 family:regulators of cell death. Annu Rev Immunol,1998,16:395-419.
[26]Lam M, Dubyak G, ChenL,et al. Evidence that Bcl-2 represses apoptosis by regulating Endoplasmic reticulnm-associates Ca2+ fluxes. Proe Natl Acad Sci USA,1994,91(14):6569-6573.
[27]Tsujimoto Y, Shimizu S. The Bcl-2 family:life-or-death switch. FEBS Lett, 2000,466(1):6-10.
[28]Haunstetter A,Izumo S. Apoptosis basic mechanisms and implications for cardio va scular disease. Circulation Research,1998,82(11):1111-1129.
[29]杜敏逸,纪方,吴新民.在体外乳鼠心肌细胞缺氧的损伤及利多卡因的保护作用.中华麻醉学杂志,1999,19(3)：161-163.
[30]VanEmous JG, Nederhoff MGJ, Ruigrok TJC, et al. The role ofthe Naq channel in the accumulation of intracellular Naq during myocardial ischemia: consequences for postischemic recovery. J Mol Cell Cardiol,1997,29(1):85-96.
[31]Matsubara T, Ishibashi T, Nakazawa M, ct al. Effects oflidocaine on ischemic myocardial metabolism assessed by 31P-NMR in the isolated perfused rat heart. Jpn Heart J,1991; 32(4):493-504.
[32]Nishikawa S, Tatsumi T, Shiraishi J, et al. Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis. J Mol Cell Cardiol,2006,40(4):510-519.
[33]Cheng W, Kajstura J, Nitahara JA, et al. Programmed myocyte cell death affects the viable myocardium after infarction in rats. Exp Cell Res,1996; 226(2): 316-27.
[34]Diwan A, Krenz M, Syed FM, et al. Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice. J Clin Invest,2007,117(10):2825-2833.
[35]Pchejetski D, Kunduzova O, Dayon A, et al. Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis. Circ Res,2007,100(1):41-49.
[36]Donath S, Li P, Willenbockel C, et al. Apoptosis repressor with caspase recruitment domain is required for cardioprotection in response to biomechanical and ischemic stress. Circulation,2006,113(9):1203-1212.
[37]Soeki T, Tamura Y, Shinohara H, et al. Relation between circulating soluble Fas ligand and subsequent ventricular remodelling following myocardial infarction. Heart,2003,89(3):339-341.
[38]Davis ME, Hsieh PC, Takahashi T, Tomosaburo Takahashi, et al. Local myocardial insulin-like growth factor 1 (IGF-1) delivery with biotinylated peptide nanofibers improves cell therapy for myocardial infarction. Proc Natl Acad Sci USA,2006,103(21):8155-8160.
[39]Das A, Xi L, Kukreja RC. Phosphodiesterase-5 inhibitor sildenafil preconditions adult cardiac myocytes against necrosis and apoptosis. Essential role of nitric oxide signaling. J Biol Chem,2005,280(13):12944-12955.
[40]Chen SJ, Bradley M, Lee, TC. Chemical hypoxia triggers apoptosis of cultured neonatal rat cardiac myocytes modulation by calium-regulated proteases and protein kinases. Mol Cell Bichem,1998,178(1-2):141-149.
[41]Pachl J, Duska F, Waldauf P, et al. Apoptosis as an early event in the development of multiple organ failure? Physiol Res,2005,586(3):697-699.
[42]Abbate A, Salloum FN, Vecile E, et al. Anakinra a recombinant human interleukin-1 receptor antagonist, inhibits apoptosis in experimental acute myocardial infarction. Circulation,2008,117(20):2670-2683.
[43]Moolman JA., Hartley S, Van Wyk J, et al. Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK. Cardiovasc Drugs Ther,2006,20(1):13-25.
[44]Liang JC, Chen HR, Chiu CC, et al. Protective effect of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker, on myocardial apoptosis in ischemia-reperfusion injury. Life Sci,2006,79(13):1248-1256.
[45]Zhang HF, Fan Q, Qian XX, et al. Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion.Apoptosis,2004,9(6):777-783.
[46]徐鹏霄,李全辉,徐健.卡托普利对高血压大鼠心、脑微血管内皮细胞Bax、Bcl-2表达的影响.2008,19(3)：203-205.
[47]Hou YP, Wu JL, Fan Q, et al. Plasma concentration of Fas/Fas ligand and left ventricular function in response to metoprolol in conjunction with standard treatment. Clinical Science,2006,112(5):299-304.
[48]Miyuki Kobara, Tetsuya Tatsumi, Daisuke Kambayashi et al. Effects of ACE Inh ibition on Myocardial Apoptosis in an Ischemia-ReperfusionR at Heart Model. J Cardiovasc Pharmacol 2003,41(6):880-889.
[49]李劲迈,朱清,岳欣等.卡托普利和氯沙坦对血管紧张素Ⅱ诱导血管平滑肌细胞Bcl-2和Fas基因表达的抑制作用.山东大学学报(医学版),2009,47(12)：25-29.
[50]耿召华,刘春燕,彭佑华,等.卡维地洛与培哚普利联合干预心肌梗死后心力衰竭对心肌细胞凋亡和肌浆网Ca+泵活性的影响.第四军医大学学报,2009,30(12)：1076-1079.
[51]Tamba M, Torreggiani A. Free radical scavenging and copper chelation:a potentially beneficial action of captopril. Free Radic Res,2000,32(3):199-211.
[52]宋陈芳,熊世熙,尹学恩,等.几种ACEI对实验性糖尿病大鼠心肌细胞凋亡和Caspase-3及Fas、FasL基因表达影响的类效应.武汉大学学报(医学版),2008,29(1)：24-27.
[53]麦炜颐,马莉,黄裕立,等.ACE抑制剂Ramipril对大鼠急性心肌梗死后心肌细胞凋亡和左室重构的影响.中山大学学报(医学科学版),2008,29(5)：550-555.
[54]耿召华,刘春燕,彭佑华,等.卡维地洛与培哚普利联合干预心肌梗死后心力衰竭对心肌细胞凋亡和肌浆网Ca2+泵活性的影响.第四军医大学学报,2009,30(12)：1076-1079.
[55]Dagenais GR, Pogue J, Fox K, et al. Angiotensin-converting enzyme inhibitors in stable vascular disease without left ventricular systolic dysfunction or heart failure:a combined analysis of three trials. Lancet,2006,368(9535):581-588
[56]邓昭武,任江华,宋爱华.缬沙坦和贝那普利对充血性心力衰竭患者细胞凋亡相关因子影响的比较.临床心血管病杂志,2007,23(10)：762-765.
[57]Odaka C, Mizuochi T. Angiotensin-converting enzyme inhibitor captopril prevents activation-induced apoptosis by interfering with T cell activation signals. Clin Exp Immunol,2000,121(3):515-22.
[58]Liu L, for the Chinese Cardiac Study (CCS-1) Collaborative Group. Long-term mortality in patients with myocardial infarction:impact of early treatment with captopril for 4 weeks. Chin Med J,2001,114(2):115-118.
[59]Ambrosioni E, Borghi C, Magnani B, for the Survival of Myocardial Infarction Long-term Evaluation (SMILE) study investigators. The effect of the angiotensin-converting-enzyme inhibitor zofenopril on mortality and morbidity after anterior myocardial infarction. N Engl J Med,1995,332(2):80-85.
[60]ACE Inhibitor Myocardial Infarction Collaborative Group. Indications for ACE inhibitors in the early treatment of acute myocardial infarction:systemic overview of individual data from 100,000 patients in randomized trials. Circulation,1998, 97(22):2202-2212.
[61]Ferrario CM, Strawn WB. Role of the Renin-Angiotensin-Aldosterone System and Proinflammatory Mediators in Cardiovascular Disease. Am J Cardiol,2006, 98(1):121-128.
[62]Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: results of the survival and ventricular enlargement trial. N Engl J Med,1992, 327(10):669-677.
[63]Kober L, Torp-Pedersen C, Carlsen JE, et al. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. New Engl J Med,1995, 333(25):1670-1676.
[64]Flather MD, Yusuf S, Kober L, et al. Long-term ACEI inhibitor therapy in patients with heart failure or left-ventricular dysfunction:a systemic overview of data from individual patients. Lancet,2000,355(9215):1575-1581.
[1]Malik V, Kale SC, Chowdhury UK, et al. Myocardial injury in coronary artery bypass grafting:On-pump versus off-pump comparison by measuring heart-type fatty-acid-binding protein release. Tex Heart Inst J.2006,33(3):321-327.
[2]Shim JK, Chio SH, Oh YJ, et al. The effect of mannitol on oxygenation and creatine kinase MB release in patients undergoing multivessel off-pump coronary artery bypass surgery. J Thorac Cardiovasc Surg,2007,133(3): 704-709.
[3]Kersten JR, Schmeling TJ, Pagel PS, et al. Isoflurane mimics ischemic preconditioning via activation of K(ATP)channels:reduction of myocardial infarct size with all acute memoryphase. Anesthesiology,1997,87(1):361-370.
[4]Weber NC, Schlack W. Inhalational anaesthetics and cardioprotection. Handb Exp Pharmacol.2008,182:187-207.
[5]Pascal C, Paul S, John G,et al. Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction in rabbits. Anesthesiology,2004,101(11):1160-1166.
[6]王钧,曾因明,李红.氟烷和异氟醚对缺血再灌注心肌收缩功能和ATP含量的影响.临床麻醉学杂志,1998,14(6)：335-337.
[7]李恒,杨承祥,孙凯等.挥发性麻醉药对大鼠离体心脏缺血再灌注损伤的影响. 中国病理生理杂志,2007,23(10)：891-895.
[8]Hannon JD, Cody MJ. Effects of volatile anesthetics on sarcolemmal calcium transport and sarcop lasmic reticulum calcium content in isolated myocytes. Anesthesiology,2002,96 (6):1457-1464.
[9]Lee MC, Chen CH, Kuo MC, et al. Isoflurane preconditioning induced cardio protection in patients undergoing coronary artery bypass grafting. Eur J Anaesthesiol,2006,23(10):841-847.
[10]Piriou V, Chiari P, Lhuillier F, et al. Pharmacological preconditioning: comparison of desflurane, sevoflurane, isoflurane and halothane in rabbit myocardium. Br J Anaesth,2002,89 (3):486-491.
[11]Hartley CJ, Reddy AK, Madala S, et al. Effects of isoflurane on coronary blood flow velocity in young, Old and ApoE(-/-)mice measured by doppler Ultrasound. Ultrasound Med Biol,2007,33(4):512-521.
[12]Tanaka K, Kawano T, Nakamura A, et al. Isoflurane activates sarcolemmal adenosine triphosphate-sensitive potassium channels in vascular smooth muscle cells. Anesthesiology,2007,106(5):984-991.
[13]Tsutsumi YM, Yokoyama T, Horikawa Y, et al. Reactive oxygen species trigger ischemic and pharmacological postconditioning:in vivo and in vitro characterization. Life Sci,2007,81 (15):1223-1227.
[14]张雪松,曾繁荣,左会明.乳化异氟醚预处理对缺血再灌注大鼠心肌的保护作用.中国康复理论与实践,2008,14(8)：727-728.
[15]李勇,魏继承.异氟醚心肌保护作用机制与临床应用西南军医,2009,11(4)： 737-739.
[16]Wei GZ, Zhou JJ,Wang B, et al. Diastolic Ca2+overload caused by Na+/Ca2+ exchanger during the firstminutes of reperfusion results in continued myocardial stunning. Eur J Pharmacol,2007,572 (1):1.11.
[17]Piper HM, Kasseckert SA, Schluter KD, et al. Pathophysiology of myocardial reperfusion injury. DtshMedWochenchr,2008,133 (12):586-590.
[18]Yildirim V, Doganci S, Aydin A,et al. Cardioprotective effects of sevoflurane, isoflurane, and propofol in coronary surgery patients:a randomized controlled study. Heart Surg Forum,2009,12(1):E1-9.
[19]Raphael J, Zuo Z, Abedat S,et al. isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin. Anesthesiology,2008,
108(3):415-425.
[20]An JZ, Bosnjak ZJ, Jiang MT. Myocardial protection by Isoflurane preconditioning Preserves Ca2+cycling proteins independent of sarcolemmal and mito-chondrial KATP channels.Anesth Analg,2007,105(5):1207-1213.
[21]Chen Q, Camara AK, An J, et al. Sevoflurane p reconditioning before moderated hypothermic ischemia p rotects against cytosolic [Ca2+] loading and myocardial damage in part via mitochondial KATP channels. Anesthesiology, 2002,97(4):912-920.
[22]Turner LA, Fujimoto K, Suzuki A, et al.The interaction of isoflurane and protein kinase C-activators on sarcolemmal KATP channels.Anesth Analg,2005, 100(6):1680-1686.
[23]Marinovic J, Bosnjak ZJ, Stadnicka A, et al. Preconditioning by isoflurane induces lasting sensitization of the cardiac sarcolemmal adenosine triphosphate-sensitive potassium channel by a protein kinase C-δ-mediated mechanism. Anesthesiology,2005,103(3):540-547.
[24]谭嵘,徐军美,冯华,等.异氟醚麻醉对体外循环心脏瓣膜置换术病人心肌的保护作用. 中华麻醉学杂志,2005,25(4)：316-318.
[25]曹德权,陈艳平,常业恬.异氟醚预处理对心脏瓣膜置换术病人血清一氧化氮与肌钙蛋白Ⅰ的影响. 临床麻醉学杂志,2006,22(7)：493-495.
[26]Varadarajan SG, An J, Novalija E, et al. Sevoflurane before or after ischemia improves cont ractile and metabolic function while reducing myoplasmic Ca2+ loading in intact hearts. Anesthesiology,2002,96(1):125-133.
[27]Stadnicka A, Marinovic J, Ljubkovic M, et al. Volatile anesthetic-induced cardiac preconditioning. J Anesth,2007,21(2):212-219.
[28]Patel H H, Gross E R, Peart J N, et al. Sarcolemmal KATP channel triggers delayed ischemic preconditioning in rats. Am J Physiol Heart Circ Physiol,2005, 288 (1):H445-7.
[29]Mykytenko J, Reeves J G, Kin H, et al. Persistent beneficial effect of postconditioning against infarct size:role of mitochondrial K(ATP) channels during reperfusion. B asic Res Cardiol,2008,103 (5):472-84.
[30]杨孟昌,陈玉培,张文胜,等.ATP敏感性钾通道在乳化异氟醚心肌保护效应中的作用.中国药理学通报,2009,25(2)：169-172.
[31]Krolikowski JG, BienengraeberM, et al. Inhibition of mitochondrial permeability transition enhances isoflurane2induced cardiop rotection during early reperfusion: the role of mitochondrial KATP channels. Anesth Analg,2005,101 (6) 1590-1561.
[32]Kwok WM, Martinelli AT, Fujimoto K, et al. Differentialmodulation of the cardiac adenosine tripbosphate sensitive potassimn channel by isoflurane and halothane. Anesthesiology,2002,97 (1):50-56.
[33]Sakai K, Zhang S,Ureshino H, et al. Interaction of isoflurane and cromakalim, a KATP channel opener, on coronary and systemic haemodynamics in chronically instrumented dogs. Acta Anaesthesiol Scand,2000,44 (9):1122-1127.
[34]张雷,顾尔伟,刘训芹,等.乳化异氟醚后处理对兔在体心脏缺血/再灌注损伤的保护作用.中国药理学通报,2009,25(10)：1322-1326.
[35]Raphael J, Zuo Z, Abedat S,et al.isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin. Anesthesiology, 2008; 108(3):415-425.
[36]Zhao ZQ, Corvera JS, HalkosME, et al. Inhibition of myocardial injury. by ischemic post conditioning during reperfusion:Comparison with ischemic p recond itioning. Am J Circ Physiol,2003,285(2):H579-H588.
[37]Belbomme D,Peynet J,Louzy M,David HM. Evidence for preconditioning by isoflurane in coronary artery bypass graft surgery. Circulation,2000,101(10)：11340-11344.
[38]RAN ke, DUAN Kai-ming, ZOU Ding-quan, et al. Protective effects of isoflurane delayed preconditioning on rabbit myocardium after ischemic-reperfusion. CLINICAL MEDICINE,2007,27 (10):69-72.
[39]张明香,刘尚国.异氟醚在非体外循环冠状动脉搭桥术中心肌保护作用的临床研究.中国煤炭工业医学杂志,2005,8(8)：892-893.
[40]Hein M, Roehl AB, Baumert JH, et al. Establishment of a porcine right ventricular infarction model for cardioprotective actions of xenon and isoflurane. Acta Anaesthesiol Scand.2008;52(9):1194-1203.
[41]Weber NC, Kandker JC, Schlack W, et al. Intermitted pharmacologic pretreatment by xenon, isoflurane, nitrous oxide, and the opioid morphine prevents tumor necrosis factor alphainduced adhesion molecule expression in human umbilical vein endothelial cells. Anesthesiology,2008,108(2):199-207.
[42]Wippermann J, Albes JM, Hartrumpf, et al. Comparison of minimally invasive closed circuit extracorporeal circulation with conventional
cardiopulmonary bypass and with off-pump technique in CABG patients: selected parameters of coagulation and inflammatory system. Eur J Cardiothorac Surg,2005,28(1):127-132[43]胡国昌,曾因明.异氟醚抑制冠状循环的中性粒细胞-内皮细胞相互作用.Anesthesia and Analgesia,2002,94 (8):49-56.
[44]阮文燕,徐军美,金丽艳,等.异氟醚预处理对心脏瓣膜置换术病人血肌红蛋白、vWF和心肌细胞显微结构的影响.中国新药与临床杂志,2009,28(11)：819-824.
[45]Harada N,Miura T,Dairaku Y, et al. NO donor-activated PKC-8 plays a pivotal role in ischemic myocardial protection through accelerated opening of mitochondrial K-ATP channels. J Cardiovasc Pharmacol,2004,44 (1):35-41
[46]Kuno A, Critz SD, Cohen MV, et al. Nicorandil opens mitochondrial K (ATP)channels not only directly but also through a NO-PKG-dependent pathway.Basic Res Cardiol,2007,102 (1):73-79.
[47]李进,袁世荧,丰新民.诱导型一氧化氮合酶在异氟醚延迟相预处理心肌保护中的作用.临床麻醉学杂志,2008,24(10)：676-678.
[48]曹德权,陈艳平,常业恬.异氟醚预处理对心脏瓣膜置换术病人血清一氧化氮与肌钙蛋白Ⅰ的影响.临床麻醉学杂志,2006,22(7)：493-495.
[49]Pravdic D, Sedlic F, Mio Y, et al. Anesthetic-induced preconditioning delays opening of mitochondrial permeability transition pore via protein Kinase C-epsilon-mediated pathway. Anesthesiology.2009,111 (2):267-74.
[50]Krolikowski JG, Weihrauch D, Bienengraeber M et al. Role of Erkl/2, p70s6K, and eNOS in isoflurane-induced cardioprotection during early reperfusion in vivo. Can J Anaesth,2006,53(2):174-182.
[51]Newberg LA, Michenfelder JD. Cerebral protection by isoflurane during hypoxemia or ischemia. Anesthesiology,1983,59(1):29-35.
[52]Hanouz JL, Yvon A, MassettiM, et al. Mechanisms of desflurane-induced p reconditioning in isolated human right atria in vitro. Anesthesiology,2002,97 (1):33-41.
[53]Tas PW, Eisemann C, Roewer N. The volatile anesthetic isoflurane suppresses spontaneous calcium oscillations in vitro in rat hippocampal neurons by activation of adenosine Al receptors. Neurosci Lett,2003,338 (3):229-232.
[54]Zheng S, Zuo Z. Isoflurane preconditioning decreases glutamate receptor overactivation-induced Purkinje neuronal injury in rat cerebellar slices.Brain Res, 2005,1054 (2):143-151.
[55]MoeMC, Berg JJ, Larsen GA, et al. The effect of isoflurane and sevoflurane on cerebrocortical presynaptic Ca2+and protein kinase C activity. NeurosurgAnesthediol,2003,15 (3):209-214.
[56]Kapinya KJ, Lowl D, Futterer C, et al. Tolerance against ischemic neuronal injury can be induced by volatile anesthetics and is inducible NO synthase dependent.Stroke,2002,33 (7):1889-1898.
[57]Xiong L Z, Zheng Y,Wu BI, et al. Preconditioning with Isoflurane Produces Dose-Dependent Neuroprotection via Activation of Adenosine Triphosphate-Regulated Potassium Channels After Focal Cerebral Ischemia in Rats. Aneath Analg,2003,96(1):233-237.
[58]李继庆,张联峰,王洋松,等.异氟醚预处理对大鼠全脑缺血再灌注损伤的保护作用.中华麻醉学杂志,2003,20(7)：515-517.
[59]吴春明,熊利泽,朱正华,等.异氟醚预处理脑保护作用的剂量-效应关系.第四军医大学学报,2002,23(15)：1357-1359.
[60]王胜,王志萍,张兆航,等.异氟醚预处理通过激活MAPK信号通路产生对离体大鼠脑的神经保护作用.国际麻醉学与复苏杂志,2006,27(2)：88-91.
[61]Engelhard K, Werner C, Reeker W, et al. Desflurane and isoflurane improve neurological outcome after incomplete cerebral ischemia in rats. Br J Anaesth, 1999,83(3):415-421.
[62]吴明春,熊利泽,朱正华,等.异氟醚预处理脑保护作用的剂量-效应关系.第四军医大学学报,2002,23(15)：1357-1359.
[63]刘艳红,熊利泽,陈绍洋,等.钠离子通道在异氟醚预处理诱导的脑保护中的作用.第四军医大学学报,2002,23(15)：1366-1368.
[64]刘艳红,熊利泽,王强,等.异氟醚预处理对大鼠脑缺血/再灌注损伤细胞内游离钙的影响.中国临床药理学与治疗学,2005,10(8)：909-912.
[65]Kudo M, Aono M, Lee Y, et al. Absence of direct antioxidant effects from volatile anesthetics in primary mixed neuronal-glial cultures. Anesthesiology, 2001,94(2):303-312.
[66]段开明,欧阳文,夏月峰,等.异氟醚麻醉对大鼠海马蛋白质组的影响.临床麻醉学杂志,2008,24(3)：239-241.
[67]Sullivan BL,Leu D, Taylor DM, et al. Isoflurane prevents delayed cell death in an organotypic slice culture model cerebral ischemia. Anesthesiology,2002,96 (1):189-195.
[68]沈洁,陈卫民.一氧化氮在异氟烷预处理脑保护中的作用.中国现代医学杂志,2007,17(21).2593-2596.
[69]Ito T, Deng X, Carr B, et al. Bel-2 phosphorylation required for anti-apoptosis function. J Biol Chem,1997,272 (18):11671-11673.
[70]孙永海,岳云,王云.再灌注期吸入异氟醚对不同程度大鼠脑缺血再灌注损伤的影响.中华麻醉学杂志.2004,24(12)：901-904.
[71]邵建林,朱俊超,吴滨阳,等.异氟醚、七氟醚和地氟醚预处理对脑缺血再灌注损伤大鼠海马CBS/H2S、iNOS/NO和HO-1/CO的影响.中华麻醉学杂志,2006,26(6)：907-910.
[72]Sullivan B L, Leu D, Taylor D M, et al. Isoflurane prevents delayed cell death in an organotypic slice culture model of cerebral ischemia. Anesthesiology,2002, 96(1):189-195.
[73]沈洁,吴兴茂,陈卫民.异氟烷预处理对缺血再灌注损伤鼠脑组织中Bcl-2和Bax的mRNA表达的影响.中国医科大学学报,2007,6(2)：138-140.
[74]李继庆,李志学,张联峰,等.异氟烷预处理对大鼠全脑缺血再灌注损伤保护机制的研究.哈尔滨医科大学学报,2004,38(6)：522-525.
[75]Johnson GL, Lapadat R. Mitogen-activated protein kinase pathwaysmediated by ERK, JNK, and p38 protein kinases. Science,2002,298 (1):1911-1912.
[76]Zheng S, Zuo Z. Isoflurane Preconditioning Induces Neuroprotection against Ischemia via Activation of P38 Mitogen-Activated Protein Kinases.Mol Pharmacol,2004,65 (5):1172-1180.
[77]Wise-Faberowski L, Pearlstein RD, Warner DS.NMDA-induced apoptosis in mixed neuronal/glial cortical cell cultures:the effects of isoflurane and dizocilpine. Neurosurg Anesthesiol,2006,18(4):240-246.
[78]黄戈.体外循环与肺保护.医学研究生报,2004,17(3)：2732-2751.
[79]陈艳平,曹德权,常业恬.异氟醚对家兔肺缺血再灌注损伤的影响.中华麻醉学杂志,2001,8(21)：483-486.
[80]王婷,蒋豪,薛张纲,等.异氟醚对大鼠肺缺血-再灌注损伤的影响.临床麻醉学杂志,2005,21(10)：713-715.
[81]王井,蒋豪,薛张纲,等.异氟醚对大鼠肺缺血再灌注损伤的保护作用.中华麻醉学杂志,2006,26(2)：140-143.
[82]王婷,蒋豪,薛张纲,等.异氟醚对大鼠肺缺血再灌注损伤时NF-κB及中性粒细胞趋化因子表达的影响.复旦学报(医学版),2005,32(4)：394-400.
[83]赵黎丽,徐道妙,覃军.异氟醚预处理对犬体外循环肺损伤的保护作用.中南 大学学报(医学版)2005,30(5)：620-621.
[84]Reutershan J, Chang D, Hayes JK, et al. Protective effects of isoflurane p retreatment in endotoxin induced lung injury. Anesthesiology,2006,104(3): 511-517.
[85]Giraud O,Molliex S, Rolland C, et al. Halogenated anesthetics reduce interleukin-1 [beta]-induced cytokine secretion by rat alveolar type II cells in primary culture. Anesthesiology,2003,98 (1):74-81.
[86]安海燕,杨拔贤.不同浓度异氟烷吸入对大鼠炎症反应的影响.山东医药,2009,49(11)：24-26.
[87]徐道妙,郭曲练,申建初,等犬单肺移植后肺动脉高压与血浆TXA2代谢的关系.中华麻醉学杂志,1998,18(3)：179-180.
[88]上官王宁,刘进.挥发性吸入麻醉药对肺的作用.国际麻醉学与复苏杂志,2007,28(4)：320-322.
[89]张健,叶敏,彭章龙,等.安氟醚和异氟醚对肝脏缺血再灌注损害的影响.中华麻醉学杂志,2000,20(4)：223-225.
[90]Morioka D, Kubota T, Sekido H, et al. Prostaglandin El improved the function of transplanted fatty liver in a rat reduced-size-liver transplantation model under conditions of permissible cold preservation. Liver Transpl,2003,9(1):79-86.
[91]王旭东,卢雅立,王飞,等.七氟烷和异氟烷对肝脏缺血再灌注损伤的影响.中山大学学报(医学科学版),2008,29(1)：30-33.
[92]Shah V, Kamath PS. Nitric oxide in liver transplantation:Pathobiology and clinical implications. Liver Transpl,2003,9(1):1-11.
[93]李泉,俞卫锋,徐学武,等.异氟醚减少离体鼠肝缺氧-复氧损伤.临床麻醉学杂志,2005,21(9)：618-620.
[94]徐广民,陶国才,易斌.异氟烷对大鼠肝脏缺血再灌注损伤时细胞间黏附分子-1表达的影响.第三军医大学学报,2008,30(3)：241-243.
[95]俞卫锋,李丽,徐学武,等.异氟烷改善离体鼠肝缺氧-复氧后氧供耗平衡.第二军医大学学报,2006,27(2)：200-202.
[96]Krumschnabel G, Manzl C, Schwarzbaum PJ. Importance of glycolysis for t he energetics of anoxia-tolerant and anoxia-intolerant teleost hepatocytes. Physiol Biochem Zool,2001,74:413-419.
[97]俞卫锋,李泉,曹云飞,等.异氟烷保护缺氧肝细胞的能量平衡.第二军医大学学报,2002,23(6)：614-616.
[98]郁勤燕,王祥瑞,杭燕南,等.地氟醚、七氟醚和异氟醚对猪肝血流及肝氧 供需平衡的影响.中华麻醉学杂志,2000,20(10)：624-627.
[99]李泉,俞卫锋,曹云飞,等.异氟醚对缺氧或复氧肝细胞能量平衡的保护作用.临床麻醉学杂志,2005,21(4)：257-259.
[100]李爱芝,马加海.吸入麻醉对大鼠急性肾缺血再灌注损伤的保护.医学动物防治,2009,25(4)：262-266.
[101]Lee H T, Ota-Setlik A, Fu Y, et al. Differential protective effects of volatile anesthetics against renal ischemia-reperfusion injury in vivo. Anesthesiology, 2004,101(6):1313-1324.
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