加味丹参饮预处理对大鼠心肌细胞延迟保护作用及细胞信号转导机理研究
|
摘要
目的:观察加味丹参饮(JDD)预处理对大鼠心肌细胞的延迟保护作用及其细胞信号转导机理。
方法:实验分三部分。第一部分:选用出生72h的大鼠,将培养72h的大鼠心肌细胞随机分6组。空白组正常培养;空白血清对照组加50%大鼠血清培养;含药血清对照组加含50%JDD的药物血清培养,缺氧/复氧(H/R)组予缺氧3h,再给氧1h;缺氧预处理(HPC)组、加味丹参饮预处理(JDDPC)组分别给予HPC、JDDPC,24h后再给予缺氧3h,再给氧1h。实验结束,以台盼蓝染色法观察各组细胞存活率,以比色法观察乳酸脱氢酶(LDH)、肌磷酸激酶(CK)的活性。
第二部分:将培养72h的大鼠心肌细胞随机分8组,空白组、空白血清对照组、含药血清对照组、H/R组、HPC组、JDDPC组处理同第一部分;HPC+多粘菌素B(PMB)组预处理前先加入PMB,余处理同HPC组;JDDPC+PMB组预处理前先加入PMB,余处理同JDDPC组。实验结束,以台盼蓝染色法观察各组细胞存活率,以比色法观察LDH、CK的活性,以PepTag非放射性蛋白激酶试剂盒检测蛋白激酶C(PKC)。
第三部分:将培养72h的大鼠心肌细胞随机分8组,空白组、空白血清对照组、含药血清对照组、H/R组、HPC组、JDDPC组处理同第一部分;HPC+格列本脲(GLI)组预处理前先加入GLI,余处理同HPC组;JDDPC+GLI组预处理前先加入GLI,余处理同JDDPC组。实验结束,以台盼蓝染色法观察各组细胞存活率,以比色法观察LDH、CK的活性,以Fura-2/AM为指示剂检测细胞内钙离子浓度,以RT-PCR检测热休克蛋白70mRNA(HSP70mRNA)。
结果:HPC组、JDDPC组细胞存活率明显高于H/R组(P＜0.01),LDH、CK明显低于H/R组(P＜0.01)。HPC+PMB组、HPC+GLI组细胞存活率、LDH及CK的活性与H/R组比较无显著性差异(P＞0.05)。JDDPC+PMB组、JDDPC+GLI组细胞存活率高于H/R组(P＜0.01),但低于HPC、JDDPC组(P＜0.01);LDH、CK的活性低于H/R组(P＜0.01),但高于HPC、JDDPC组(P＜0.01)。
HPC组、JDDPC组PKC的活性、HSP70mRNA表达显著高于H/R组(P＜0.01),细胞内钙离子浓度显著低于H/R组(P＜0.01)。HPC+PMB组PKC活性、HPC+GLI组HSP70mRNA及细胞内钙离子浓度与H/R组比较无显著性差异(P＞0.05)。JDDPC+PMB组PKC活性、JDDPC+GLI组HSP70mRNA表达高于H/R组(P＜0.01或P＜0.05),但低于HPC、JDDPC组(P＜0.01);JDDPC+GLI组细胞内钙离子浓度低于H/R组(P＜0.01),但高于HPC、JDDPC组(P＜0.01)。
结论:①加味丹参饮预处理具有延迟保护作用。②PKC的抑制剂PMB、ATP敏感性钾通道(K_(ATP))的抑制剂GLI能完全阻断HPC的延迟保护作用,说明PKC是HPC的信号转导通路,K_(ATP)为HPC的终末效应物,能减少钙超载,同时诱导HSP70的高表达。③PKC的抑制剂PMB、K_(ATP)的抑制剂GLI不能完全阻断加味丹参饮预处理的延迟保护作用,说明加味丹参饮预处理不完全通过PKC信号转导途径及K_(ATP)通道发挥延迟保护作用,提示加味丹参饮预处理能从多种途径、多个靶点启动心肌内源性的调控保护。
Purpose: To observe the delayed protective function of the precondition of Jiawei Danshen decoction(JDD) to the rat's myocardial cell and its cell signal transduction mechanism.
Method: The experiment contains three steps.
Step 1:
Rat that were born 72 hours ago were chosen and rat myocardial cell, which had been cultured for 72 hours, was divided at random into 6 groups. The normal group was cultured in a usual way; the serum contrast group with 50% rat serum; and the medicine-serum group with 50% medicine serum containing JDD. The Hypoxic/reoxygenation(H/R) group was made to have three-hour's hypoxia and then reoxygenated for an hour. The Hypoxic preconditioning(HPC) group and the JDD preconditioning(JDDPC) group were given HPC and JDD precondition separately. After 24 hours, both of them were made to have three-hour's hypoxia and then reoxygenated for an hour. At the end of this step, the cell survival rate of each group was identified by TB straining while LDH and CK by colorimetry.
Step 2:
The rat myocardial cell, cultured for 72 hours, was divided into 8 groups at random. The normal group, the serum contrast group, the medicine-serum contrast group, the H/R group, the HPC group and the JDDPC group were treated the same as in Step 1. The HPC+PMB group was added PMB before precondition, and its following process was the same as the HPC group. The JDDPC + PMB group was added PMB before precondition, and the following process was the same as the JDDPC group . At the end of this step, the cell survival rate of each group was identified by TB straining, LDH and CK by colormetry, and PKC by PepTag(?) non-radioactive protein kinase reagent.
Step 3:
The rat myocardial cell, cultural for 72 hours, was divided into 8 groups at random. The normal group, the serum contrast group, the medicine-serum contrast group, the H/R group, the HPC group and the JDDPC group were treated the same as in Step 1. The HPC+GLI group was added GLI before precondition, and its following process was the same as the HPC group. The JDDPC + GLI group was added GLI before precondition, and the following process was the same as the JDDPC group . At the end of this step, the cell survival rate of each group was identified by TB straining, LDH and CK by colormetry. The concentration of calcium ion inside the cell was tested by Fura-2/AM, as the indicator, and the HSP 70m RNA by RT-PCR.
Result: The cell survival rate of HPC group and JDDPC group is obviously higher than the H/R group (P<0.01), while LDH and CK lower than H/R group (P<0.01). The cell survival rate, LDH and CK of HPC+PMB group and HPC+GLI group are similar to the H/R group (P>0.05). The cell survival rate of JDDPC + PMB group and JDD PC+ GLI group are higher than the H/R group (P<0.01), but lower than HPC and the JDDPC group (P<0.01). The LDH and CK of them are lower than the H/R group (P<0.01), but higher than HPC and JDDPC group.
The PKC activity and HSP70mRNA of the HPC group and JDDPC group are obviously higher than H/R group (P<0.01), but the concentration of calcium ion inside the cell is obviously lower than the H/R group (P<0.01). The PKC activity of HPC+PMB group and the HSP70mRNA and concentration of calcium ion inside the cell of HPC+GLI group are similar to H/R group (P>0.05). PKC activity of the JDDPC + PMB group and HSP 70mRNA of JDDPC + GLI group are higher than H/R group (P<0.01 or P<0.05), but lower than HPC and the JDDPC group. The concentration of calcium ion inside the cell of JDD PC+ GLI group is lower than the H/R group (P<0.01), but higher than HPC and the JDDPC group (P<0.01).
Conclusion: The precondition of JDD is of delayed protective function. PMB, the inhibitor of PKC, and GLI, of K_(ATP), can completely stop the delayed protective function of HPC, which means PKC is the signal transduction pathway of HPC and K_(ATP) is the final effector, K_(ATP) can reduce calcium overloan and induce a high convey of HSP70. PMB, the inhibitor of PKC, and GLI, of K_(ATP), can not completely stop the delayed protective function of the precondition of JDD, which means the precondition of JDD does not completely play its delayed protective function through PKC signal transduction pathway and K_(ATP) pathway, indicating that there are many pathways of the signal transduction in JDDPC.
方法:实验分三部分。第一部分:选用出生72h的大鼠,将培养72h的大鼠心肌细胞随机分6组。空白组正常培养;空白血清对照组加50%大鼠血清培养;含药血清对照组加含50%JDD的药物血清培养,缺氧/复氧(H/R)组予缺氧3h,再给氧1h;缺氧预处理(HPC)组、加味丹参饮预处理(JDDPC)组分别给予HPC、JDDPC,24h后再给予缺氧3h,再给氧1h。实验结束,以台盼蓝染色法观察各组细胞存活率,以比色法观察乳酸脱氢酶(LDH)、肌磷酸激酶(CK)的活性。
第二部分:将培养72h的大鼠心肌细胞随机分8组,空白组、空白血清对照组、含药血清对照组、H/R组、HPC组、JDDPC组处理同第一部分;HPC+多粘菌素B(PMB)组预处理前先加入PMB,余处理同HPC组;JDDPC+PMB组预处理前先加入PMB,余处理同JDDPC组。实验结束,以台盼蓝染色法观察各组细胞存活率,以比色法观察LDH、CK的活性,以PepTag非放射性蛋白激酶试剂盒检测蛋白激酶C(PKC)。
第三部分:将培养72h的大鼠心肌细胞随机分8组,空白组、空白血清对照组、含药血清对照组、H/R组、HPC组、JDDPC组处理同第一部分;HPC+格列本脲(GLI)组预处理前先加入GLI,余处理同HPC组;JDDPC+GLI组预处理前先加入GLI,余处理同JDDPC组。实验结束,以台盼蓝染色法观察各组细胞存活率,以比色法观察LDH、CK的活性,以Fura-2/AM为指示剂检测细胞内钙离子浓度,以RT-PCR检测热休克蛋白70mRNA(HSP70mRNA)。
结果:HPC组、JDDPC组细胞存活率明显高于H/R组(P＜0.01),LDH、CK明显低于H/R组(P＜0.01)。HPC+PMB组、HPC+GLI组细胞存活率、LDH及CK的活性与H/R组比较无显著性差异(P＞0.05)。JDDPC+PMB组、JDDPC+GLI组细胞存活率高于H/R组(P＜0.01),但低于HPC、JDDPC组(P＜0.01);LDH、CK的活性低于H/R组(P＜0.01),但高于HPC、JDDPC组(P＜0.01)。
HPC组、JDDPC组PKC的活性、HSP70mRNA表达显著高于H/R组(P＜0.01),细胞内钙离子浓度显著低于H/R组(P＜0.01)。HPC+PMB组PKC活性、HPC+GLI组HSP70mRNA及细胞内钙离子浓度与H/R组比较无显著性差异(P＞0.05)。JDDPC+PMB组PKC活性、JDDPC+GLI组HSP70mRNA表达高于H/R组(P＜0.01或P＜0.05),但低于HPC、JDDPC组(P＜0.01);JDDPC+GLI组细胞内钙离子浓度低于H/R组(P＜0.01),但高于HPC、JDDPC组(P＜0.01)。
结论:①加味丹参饮预处理具有延迟保护作用。②PKC的抑制剂PMB、ATP敏感性钾通道(K_(ATP))的抑制剂GLI能完全阻断HPC的延迟保护作用,说明PKC是HPC的信号转导通路,K_(ATP)为HPC的终末效应物,能减少钙超载,同时诱导HSP70的高表达。③PKC的抑制剂PMB、K_(ATP)的抑制剂GLI不能完全阻断加味丹参饮预处理的延迟保护作用,说明加味丹参饮预处理不完全通过PKC信号转导途径及K_(ATP)通道发挥延迟保护作用,提示加味丹参饮预处理能从多种途径、多个靶点启动心肌内源性的调控保护。
Purpose: To observe the delayed protective function of the precondition of Jiawei Danshen decoction(JDD) to the rat's myocardial cell and its cell signal transduction mechanism.
Method: The experiment contains three steps.
Step 1:
Rat that were born 72 hours ago were chosen and rat myocardial cell, which had been cultured for 72 hours, was divided at random into 6 groups. The normal group was cultured in a usual way; the serum contrast group with 50% rat serum; and the medicine-serum group with 50% medicine serum containing JDD. The Hypoxic/reoxygenation(H/R) group was made to have three-hour's hypoxia and then reoxygenated for an hour. The Hypoxic preconditioning(HPC) group and the JDD preconditioning(JDDPC) group were given HPC and JDD precondition separately. After 24 hours, both of them were made to have three-hour's hypoxia and then reoxygenated for an hour. At the end of this step, the cell survival rate of each group was identified by TB straining while LDH and CK by colorimetry.
Step 2:
The rat myocardial cell, cultured for 72 hours, was divided into 8 groups at random. The normal group, the serum contrast group, the medicine-serum contrast group, the H/R group, the HPC group and the JDDPC group were treated the same as in Step 1. The HPC+PMB group was added PMB before precondition, and its following process was the same as the HPC group. The JDDPC + PMB group was added PMB before precondition, and the following process was the same as the JDDPC group . At the end of this step, the cell survival rate of each group was identified by TB straining, LDH and CK by colormetry, and PKC by PepTag(?) non-radioactive protein kinase reagent.
Step 3:
The rat myocardial cell, cultural for 72 hours, was divided into 8 groups at random. The normal group, the serum contrast group, the medicine-serum contrast group, the H/R group, the HPC group and the JDDPC group were treated the same as in Step 1. The HPC+GLI group was added GLI before precondition, and its following process was the same as the HPC group. The JDDPC + GLI group was added GLI before precondition, and the following process was the same as the JDDPC group . At the end of this step, the cell survival rate of each group was identified by TB straining, LDH and CK by colormetry. The concentration of calcium ion inside the cell was tested by Fura-2/AM, as the indicator, and the HSP 70m RNA by RT-PCR.
Result: The cell survival rate of HPC group and JDDPC group is obviously higher than the H/R group (P<0.01), while LDH and CK lower than H/R group (P<0.01). The cell survival rate, LDH and CK of HPC+PMB group and HPC+GLI group are similar to the H/R group (P>0.05). The cell survival rate of JDDPC + PMB group and JDD PC+ GLI group are higher than the H/R group (P<0.01), but lower than HPC and the JDDPC group (P<0.01). The LDH and CK of them are lower than the H/R group (P<0.01), but higher than HPC and JDDPC group.
The PKC activity and HSP70mRNA of the HPC group and JDDPC group are obviously higher than H/R group (P<0.01), but the concentration of calcium ion inside the cell is obviously lower than the H/R group (P<0.01). The PKC activity of HPC+PMB group and the HSP70mRNA and concentration of calcium ion inside the cell of HPC+GLI group are similar to H/R group (P>0.05). PKC activity of the JDDPC + PMB group and HSP 70mRNA of JDDPC + GLI group are higher than H/R group (P<0.01 or P<0.05), but lower than HPC and the JDDPC group. The concentration of calcium ion inside the cell of JDD PC+ GLI group is lower than the H/R group (P<0.01), but higher than HPC and the JDDPC group (P<0.01).
Conclusion: The precondition of JDD is of delayed protective function. PMB, the inhibitor of PKC, and GLI, of K_(ATP), can completely stop the delayed protective function of HPC, which means PKC is the signal transduction pathway of HPC and K_(ATP) is the final effector, K_(ATP) can reduce calcium overloan and induce a high convey of HSP70. PMB, the inhibitor of PKC, and GLI, of K_(ATP), can not completely stop the delayed protective function of the precondition of JDD, which means the precondition of JDD does not completely play its delayed protective function through PKC signal transduction pathway and K_(ATP) pathway, indicating that there are many pathways of the signal transduction in JDDPC.
引文
[1]Murry CE,Jennings RB,Reimer KA.Preconditioning with ischemia:A delay of lethal cell injury in ischemic myocardium[J].Cireulation,1986,74(5):1124
[2]朱方.缺血预处理保护心肌作用的分子生物学机制[J].心血管病学进展,1998,19(4):214
[3]梁日欣,廖福龙,韩东.川芎嗪预处理对清醒大鼠心肌缺血再灌注损伤的保护作用[J].中国实验方剂学杂志,2002,8(1):21
[4]陈锋,王成天,王焱林,等.三七总皂苷预处理对在体大鼠心肌缺血再灌注的保护作用[J].中华麻醉学杂志,2000,20(7):437
[5]张卫军,史载祥,王蓓蓓,等.大蒜素模拟心肌缺血预处理作用的研究[J].中国循环杂志,2000,15(3):140
[6]程桂荣,易胜中.黄芪预处理大鼠心肌保护效应的实验研究[J].高血压杂志,2001,9(4):326
[7]卫洪昌,王秀薇,吕嵘,等.益心口服液药物预处理对大鼠心肌缺血再灌注损伤的影响[J].药学实践杂志,2001,9(3):157
[8]黄政德,张玉生,葛金文.加味丹参饮对家兔动脉粥样硬化形成影响的研究[J].湖南中医学院学报.2002,22(4):4
[9]黄政德,葛金文,张玉生.加味丹参饮对家兔缺血再灌注损伤心肌延迟保护作用的研究[J].湖南中医杂志,2003,19(6):52
[10]徐叔云,卞如濂.药理实验方法学[M].第2版.北京:人民卫生出版社,2002,45.
[11]刘建文.药理实验方法学-新技术与新方法[M].北京:化学工业 出版社,2003.258
[12]潘启超,胥彬.肿瘤药理学与化学治疗学[M].郑州:河南医科大学出版社,2000.783.
[13]黄世敬,翁维良.冠心病辨证诊断规范化研究概况[J].辽宁中医杂志,2000,27(3):142
[14]朱明军,王永霞.CHD中医辨证研究进展[J].上海中医药大学学报,2006,20(1):72
[15]陈贵延,薛赛琴.最新国内外疾病诊疗标准[S].北京:学苑出版社,1992.209-212,678
[16]中西医结合心血管学会.CHD的中医辨证标准[S].中西医结合杂志,1991,11(5):257
[17]中华人民共和国卫生部.中药新药治疗胸痹心痛的临床研究指导原则[S].1993.41
[18]郑筱萸.中药新药临床研究指导原则[S].北京:中国医药科技出版社,2002
[19]王永炎.中医内科学[M].上海:上海科学技术出版社,1997
[20]陈可冀,张之南,梁子钧,等.血瘀证与活血化瘀研究[M].上海:上海科学技术出版社,1990.127-137
[21]刘德恒,许真真,郭伟聪.CHD心绞痛395例中医证型特点探讨[J].中医杂志,1995,35(1a):517
[22]郭志华.CHD心绞痛2432例中医辨证分型综合统计分析[J].湖南中医杂志,1998,14(2):7
[23]张秋雁,邓冰湘.CHD心绞痛临床中医证型分布的回顾性分析[J].中医研究,2005,18(11):23
[24]旷惠桃,潘远根.CHD心绞痛临床证型分类探讨[J].中医杂志,1997,38(12):742
[25]胡冬裴.胸痹证治文献研究[J].山东中医药大学学报,2005,29(1):37
[26]马晓昌,尹太英,陈可冀,等.CHD中医辨证分型与冠状动脉造影所见相关性比较研究[J].中国中西医结合杂志,2001,21(9):654
[27]张敏州,丁邦晗,张维东,等.375例胸痹心痛患者冠状动脉造影结果与中医证型的对比研究[J].中国中西医结合急救杂志,2004,11(2):115
[28]李俊,李小敏,刘映峰.冠脉狭窄程度与血脂脂蛋白及中医证型关系[J].辽宁中医杂志,1999,26(11):486
[29]赵亚莉,杨幼新.CHD心电图与中医辨证分型的关系[J].江苏中医,2001,22(9):20
[30]岑永庄,黎学松.CHD常见心律失常与中医辨证分型关系的临床研究[J].新中医,1998,30(8):34
[31]周中山.CHD心绞痛中医证型与血液流变学的相关性研究[J].湖南中医药导报,2001,7(7):360
[32]丘瑞香,罗致强.CHD血瘀证血液理化特性与中医证型相关性研究[J].中医杂志,2002,43(5):378
[33]吕芳芳,黄文.CHD心绞痛不同证型与血液流变关系的探讨[J].北京中医,2004,23(6):327
[34]蔡辉,宁静,吴利群,等.血瘀证患者甲皱微循环检测的研究[J].中国医药学报,1995,10(3):30
[35]张三林,赵京生,张海涛,等.CHD患者中医证型与甲襞微循环变化的相关性研究[J].微循环学杂志,1999,9(2):46
[36]梁东辉,尹炳生,曾昭龙,等.老年CHD痰瘀辨证与血清脂蛋白谱检测的探讨[J].中国中西医结合杂志,1999,1(3):155
[37]庄德成,朱学云,钱小奇,等.高脂血症辨证分型与血脂指标的相关性研究[J].江苏中医,2001,22(9):18
[38]袁肇凯,简亚平,黄献平,等.高脂血症痰瘀辨证的血脂和血流动力学检测分析[J].湖南中医学院学报,2001,21(3):1
[39]毛成,叶式,刘强,等.CHD中医辨证分型与胰岛素抵抗关系的初步研究[J].中国中西医结合杂志,2001,21(9):657
[40]孙锡印,杨突琳.CHD气滞血瘀与气虚血瘀型间血载脂蛋白的异同及辨治影响[J].江苏中医,1997,18(6):40
[41]张月愁,梁东辉,李小敏,等.CHD疾病辨证分型与血清血脂蛋白平衡失调的研究[J].中国中西医结合杂志,1995,15(1):9
[42]张憋,梁东辉,曾昭龙,等.CHD痰瘀辨证与血清血脂蛋白谱检测的探讨[J].中国中西医结合杂志,1999,19(3):155
[43]蔡钦朝,汪琼华,吴云智,等.血瘀证患者血管内皮内分泌功能的观察[J].安徽中医学院学报,1998,17(2):61
[44]陈云波,侯孟君,王奇,等.血瘀证兔血清对培养的血管内皮细胞活性因子基因表达的影响[J].广州中医药大学学报,2001,18(2):100
[45]刘红旭,黄丽娟,金欢.血瘀胸痹血浆内皮源性收缩/舒张因子水平及治疗影响研究[J].北京中医,1995,(6):49
[46]陈建鸿,杜建.CHD中医辨证与内皮素及降钙素基因相关肽关系的临床研究[J].中医杂志,1998,39(2):108
[47]秦鉴,金明华,邓江华,等.化湿和化瘀法治疗CHD的临床研究[J].中国中西医结合杂志,1997,17(9):519
[48]过鑫昌,丁怀翌,戚文航,等.前列腺素、血小板功能CHD中医辨证分型与蛋白C抗原的关系[J].中国中西医结合杂志,1991,11(5):263
[49]梁铁军,高顺宗,张发丽,等.CHD患者抗凝系统改变与中医证型关系[J].中国中西医结合杂志,1995,15(10):599
[50]骆丽娟.CHD证型与P-选择素、TXB2及6-Keto-PGF含量变化关系的研究[J].上海中医药杂志,2002,36(7):13
[51]吕中,祝光礼,施赛珠.CHD患者单核细胞凝血/纤溶活性改变与证型关系[J].浙江中医杂志,2002,37(1):33
[52]梁晓春,郭赛珊.前列腺素与中医中药[J].中西医结合杂志,1990,10(3):185
[53]严卉,胡晓晟,陈君柱,等.血浆同型半胱氨酸和冠状动脉粥样硬化严重程度与中医证型的关系[J].中国中西医结合杂志,2002,22(11):813
[54]中国医学科学院阜外医院等.冠心Ⅱ号治疗CHD心绞痛164例远期疗效观察[J].心血管疾病,1978,(1):22
[55]陈可冀,钱振淮,张问渠,等.精制冠心片双盲法治疗CHD心绞痛112例疗效分析[J].中华心血管杂志,1982,(2):85
[56]周小青,罗尧岳,谢小兵,等.五首活血化瘀方对实验性动脉粥样硬化家兔血脂、载脂蛋白的影响[J].中国中医药信息杂志,2003,10(4):29
[57]王瑷芬,翟雯娟.红花注射液治疗CHD心绞痛、心肌缺血临床观察[J].医学理论与实践,2003,16(9):1002
[58]高承贤,丁志山,沃兴德,等.血府逐瘀汤抗心肌缺血及耐缺氧作用的实验研究[J].浙江中医学院学报,2001,25(2):45
[59]余追,欧阳静萍,刘永明,等.当归抗家兔主动脉粥样硬化形成的作用[J].中国动脉硬化杂志,2000,8(1):46
[60]李鲁杨,任国华,刘向红,等.扶正降黏胶囊改善CHD患者血 栓前期相关因素的临床研究[J].中国中西医结合杂志,2005,25(8):691
[61]谢建安,刘新红.心血丹注射液治疗CHD患者的疗效及其对血液流变学的影响[J].陕西中医,2005,26(10):1064
[62]朱薇,贾满仓.复方丹参滴丸治疗CHD心绞痛60例临床观察[J].中国中医急症,2005,14(8):742
[63]杨永华,朱伟荣,朱建秀,等.灯盏花素治疗CHD30例临床研究[J].中西医心脑血管病杂志,2003,1(3):141
[64]黄志平,李小林,廖庆文,等.川芎嗪对CHD患者抗氧化酶、脂质过氧化物及脂肪酸含量的影响[J].中国中医药科技,2005,12(5):272
[65]赵泽红,郑祖云,范邻翔,等.补心活络胶囊对CHD及其脂质过氧化作用的影响[J].广州中医药大学学报,2002,6(2):85
[66]王昕.归芪胶囊对家兔心肌缺血-再灌注损伤中SOD,MDA,NOS 影响实验研究[J].中医药学刊,2004,22(10):1815
[67]丘瑞香,贺敬波,蓝军,等.心脉通胶囊保护血管内皮细胞损伤的临床研究[J].中国中西医结合杂志,1998,18(2):74
[68]丘瑞香,贺敬波,蓝军,等.心脉通胶囊对CHD患者心肌缺血总负荷影响及其作用机制探讨[J].中国中西医结合杂志,2000,20(1):19
[69]丘瑞香,祁翠仪,贺敬波,等.心脉通胶囊对CHD患者血管活性因子的调节作用[J].中国医药学报,1999,14(1):29
[70]汪坚敏,王俏,朱健.三七总皂苷对CHD不稳定型心绞痛内皮功能的影响[J].临床中老年保健,2002,5(3):183
[71]华宇明,管耘园,金恒,等.复方丹参对血浆内皮素和一氧化氮浓度的影响[J].中国临床药理学与治疗学,2000,5(4): 363
[72]曹静.复脉灵颗粒治疗气滞血瘀型CHD心绞痛的临床研究[J].中西医结合心脑血管病杂志,2005,3(8):673
[73]杨庆福,李彩玲,陈俭.复方丹参滴丸对CHD心绞痛患者血管内皮功能的影响[J].新乡医学院学报,2003,20(2):127
[74]黎玉,万福生,李少华,等.川芎嗪对大鼠缺血心肌线粒体NO 及自由基的影响[J].中医药学报,2004,32(2):47
[75]谭元生,邓圣明,谭超.药物预处理对缺血再灌注损伤心肌的保护作用[J].中医药学刊,2003,21(6):877
[76]梁日欣,廖福龙,韩东.川芎嗪预处理对体外培养乳鼠心肌细胞低氧再给氧损伤的保护作用[J].中药药理与临床,2000,16(6):7
[77]傅俊英,史载祥,张久亮,等.大蒜素延迟预处理对实验性兔心肌梗死损伤保护作用的研究[J].中国比较医学杂志,2005,15(4):221
[78]郭利平,高秀梅,张萌.丹酚酸B预处理的心脏微血管内皮细胞延迟保护作用研究[J].天津中医,2002,19(1):41
[79]刘颖,陈晨,吴伟康,等.四逆汤预处理对大鼠心缺血再灌注后心功能的延迟保护作用[J].中药药理与临床,2006,22(1):11
[80]Qiu Y,Ping P,Tang XL,et al.Directe vidence that protein kinase C plays an essential role in the development of late preconditioning against myocardia stunning in conscious rabbits and that epsilon is the isoform in volved[J].J Cli Invest,1998,101:2182
[81]Dawn B,Xuan YT,Qiu Y,et al.Bifunctional role of protein tyrosine kinases in late preconditioning against myocardial stunning in conscious rabbits [J].Circ Res,1999,85(12): 1154
[82] Noma A.. ATP-regulated K~+ channels in cardiacmuscle [J].Nature, 1983, 305:147
[83] Inoue I, Nagase H, Kishi K, et al. ATP-sensitive K~+ channel in the mitochondrial inner membrane[J]. Nature, 1991,352:244
[84] Liu H, Chen H, Yang X, Cheng J. ATP sensitive K~+ channel may be involved in the protective effects of preconditioning in isolated guinea pig cardiomyocytes [J].Chin Med J(Engl), 2001, 114(2): 178
[85] Kukreja RC. Role of K_(ATP) channel in heart and pharmacological preconditioning[J]. Ann N Y Acad Sci, 1999, 874: 211-221.
[86] Zhao T C,Hines D S,Kukreja R C.Adenosine induced late preconditioning in the mouse hearts:Role p38MAP kinase and mitochondrial K_(ATP) channels [J]. Am J Physiol,2001, 280: 1278
[87] Takano H, Bolli R, Black R G, et al. Al or A3 receptors induce late preconditioning against infarction in conscious rabbits by different mechanisms [J]. Cir Res,2001,88:520
[88] Schultz JJ, Hsu A K, Nagase H, et al.TAN-67, a deltal-opioid receptor agonist, reduces infarct size via activity of Gi/o protein and K_(ATP) channels[J]. Am J Physiol, 1998,274 (3pt2): 909
[89] Zhao TC, Hines DS, Kukreja RC. Adenosine-induced late preconditioning in mouse hearts: role of p38 MAP kinase and mitochondrial KATP channels[J]. Am J Physiol Heart Circ Physiol, 2001, 280: 1278
[90] Fryer RM, Hsu AK, Eel Is JT, et al. Opioid-induced second window of cardioprotection potential role of mitochondrial K_(ATP) channels [J]. Circ Res, 1999, 84:846
[91] Liana BT.Direct preconditioning of cardiac ventricular myocytes via adenosine Al receptor end KATP channel[J].Am J physiol. 1996 Nov;271 (SPt2): 1769
[92] Cleveland JC Jr, Meldrvm DR, Rowland RT,et al.Adenosine preconditioning of human myocardium is dependent upon theATP-sensitive K~+ channel[J].J Mol Cell Cardiol, 1997,29(1): 175
[93] Jiang BT. Protein kinase C-mediated preconditioning of cardiac myocytes: role of adenosine receptor and K_(ATP) channel[J]. Am J Physiol, 1997, 273 (2pt2): 847
[94] Zhuang JG, Zhang Y, Zhou ZN. Hypoxic preconditioning upregulates KATPchannels through activation of protein kinase C in rat ventricular myocytes[J].ACTAPHARMACOLOGICA SINICA, 2000, 21 (9): 845
[95] Wang Y, Hirai K, Ashraf M. Activation of mitochondrial ATP-sensitive K~+ channel for cardiac protection against ischemic injury is dependent on protein kinase Cactivity[J].Circ Res, 1999, 85: 731
[96] Fryer RM, Eells JT, Hsu AK, et al . Ischemic preconditioning in rats: role of mi tochondr ial K_(ATP) channel in preservation of mitochondrial function[J]. Am J Physiol Heart Circ Physiol, 2000, 278:305
[97] Brain. Myocardial KATP channels in preconditioning [J].Circ Res, 2000, 87:845
[98] Korge P,Honda HM,Weiss JN.Protection of cardiac mitochondria by diazoxide and protein kinase C: implications for ischemic precondi tioning [J]. Proc Natl Acad Sci USA, 2002, 99: 33122
[99] de Klaver MJM, Manning L, Palmer LA, et al. Isaflurane Pretreatment Inhibits Cytokine — induced Cell Death in Cultured Rat Smooth Muscle Cells and Human Endothelial Cells [J]. Anesthesiology, 2002, 97:24
[100] Beresewicz A, Maczewski M, Duda M. Effect of classic preconditioning and diazoxide on endothelial function and O~(2-) and NO generation in the post-ischemic guinea-pig heart[J]. Cardiovascular Research, 2004, 63: 118
[101] Maczewski M, Duda M, Pawlak W, et al. Endothelial protection from reperfusion injury by ischemic preconditioning and diazoxide involves a SOD—1 ike anti-02-mechanism[J]. J Physiol Pharmacol, 2004, 55:537
[102] Toyoda Y, Friehs I, Parker RA, et al. Differential role of sarcolemmal and mi tochondrial K_(ATP) channels in adenosine enhanced ischemia preconditioning[J]. Am J Phys Circ Physiol, 2000, 279:2694
[103] Pain T, Yang XM, Stuart D, et al. Opening mi tochondrial K_(ATP) channel triggers the percondit ioned state by generating free radicals[J]. Circ Res, 2000, 87:460-466
[104] Stowe DF, Kevin LG. Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics[J]. Antioxid Redox Signal,2004, 6:439
[105] Vanden Hoek TL, Becker LB, Shao Z, et al . Reactive oxygen species released from mitochondria during brief hypoxia induce preconditioning in cardiomyocytes[J]. J Biol Chem, 1998, 273: 18092
[106] Murata M, Akao M, O. Rourke B , et al. Mitochondrial ATP-sensitive potassium channels attenuate matrix Ca~(2+) over load during simulated ischemia and reperfusion: possible mechanism of cardioprotection[J]. CircRes, 2001, 89: 891
[107] Cuevas P,Carceller F,Martinez-CosoV, et al.Fibroblast growth factor cardioprotection against ischemia-reperfusion injury may involve K~+ ATP channels[J].Eur J Med Res, 2000, 5: 145
[108] Polakowski JS, Wegner CD, Cox BF. Bimoclomol elevates heat Shock protein 70 and cytoprotects rat neonatal cardiomyocytes. Eur J Pharmacol, 2002, 435(1): 73
[109] Yellen DM. Baxter GF. A "second window of protection" or delayed preconditioning phenomenon: future horizons for myocardial protection[J]? J Mol Cell Cardiol,1995,27: 1023
[110] Yamashita N, Nishida M, Hoshida S, et al. Induction of manganese superoxide dismutation in rat cardiac myocytes increase tolerance to hypoxia 24 hours after precondioning[J].J Clin lovest,1994,94:2193
[111]刘秀华,陈奎,武旭东,等.缺血预处理的普遍性[J].北京医科大学学报,1996,28:170
[112]Zhou X,Zhai X.Astral M.Direct evidence that initial oxidative stress triggered by preconditioning contributes to second window of protection by endogenous antioxidant enzyme in myocytes[J].Circulation,1996,93:1177
[113]Latchman DS.Heat shock proteins and cardiacpro-tection [J].Cardiovasc Res,2001,51(4):637-646
[114]Craig EA,Weissman IS.Homich AL.Heat shock protein and molecular chaperones:mediators of protein conformation and turnover in the cell[J].Cell,1994,78:491
[115]Marber MS,Mestril R,Chi S-H,et al.Over expression of the rat inducible 70-kDa heat stress protein in transgenic mouse increases the resistance of the heart to ischemic injury[J].J Clin Invest,1995,95(4):1446
[116]Latchman DS.Heat shock protein and cadiac protection[J].Cardiovasc-Res[J].2001,51(4):637
[117]Engel man DT,Chen CZ,Watanabe M,et al.Improved 4-and 6-hour myocardial preservation by hypoxic preconditioning[J].Circulation.1995,92(9Suppl):417
[118]Knowltor AA,Bercher P,Apstein CS.Rapid expression of heat shock protein in the rabbit after brief cardiac ischemia[J]. 7 Clin Invest. 1991,-87: 139
[119] Marber MS, Latchman DS, Walker JM, et al. Cardiac stress protein elevation 24 hour s after brief ischemia or heart stress is associated with resistance to myocardial infarction[J]. Circulation, 1993, 89:1264
[120] Zhou JJ, Pei JM, Wang GY. Inducible HSP70 mediates delayed cardio-protection via U-5048H pretreatment in rat ventricular myocytes[J].AmJ Physiol Heart Cire Physiol,2001, 281(1): 40
[1]金惠铭,卢建,殷莲华.细胞分子病理生理学[M].郑州:郑州大学出版社,2002.565
[2]Kudo M,Wang YG,Xu MF,et al.A denosine A(1) receptor mediates late preconditioning via activation of PKC-delta signaling pathway[J].Am J Physiol Heart Cire Physiol,2002,283(1):296
[3]DanaA,BaxterGF,WalkerJM,et al.Prolonging the delayed phase of myocardial protection:repetitive adenosine Al receptor activation maintains rabbit myocardium in a preconditioning statec[J].J Am Coll Cardiol,1998,31:1142
[4]Bolli R,Bhatti ZA,Tang XL,et al.Evidence that late preconditioning against myocardial stunning in conscious rabbits is triggered by the generation of nitric oxide[J].Circ Res,1997,81:42
[5]Banerjee S,Tang XL,Qiu Y.Nitroglycerin induces late preconditioning against myocardial stunning via a PKC-dependent path way[J].Am J Physiol Heart Circ Physiol,1997,81:2488
[6]Imagawa J,Yellon DM,Baxter GF.Pharmacological evidence that inducible nitric oxide synthesis is a mediator of delayed preconditioning[J].Br J Pharmacol,1999,126:701
[7]Sasaki N,Sato T,Ohler A,et al.Activation of mitochondrial ATP-dependent potassium channels by nitric oxide[J].Circulation,2000,101:439
[8]Shinmura K,Tang XL,Takano H,et al.Nitric oxide donors attenuate myocardial stunning in conscious rabbits[J].Am J Physiol,1999,277(6Pt2):H2495
[9]Takano H,Tang XL,Qiu Y,et al.Nitric oxide donors induce late preconditioning against myocardial stunning and infarction in conscious rabbits via an antioxidant-sensitive mechanism[J].Cire Res,1998,83:73
[10]Zhou FW,Li YJ,Deng HW.Early and delayed protection by capsaicinagains reperfusion in jury in rat heart[J].Acta Pharmacol Sin,1999,20:912
[11]Song QJ,Li.YJ,Deng HW.Early and delayed cardioprotection by heat stress is mediated by calcitonin gene-related peptide[J].Naunyn Schmiedebergs Arch Pharmacol,1999,359:477
[12]Peart JN,Gross GJ.Chronic exposure to morphine produces a marked cardioprotective phenotype in aged mouse hearts[J].Exp Gerontol,2004,39(7):1021
[13]Fryer RM,Hsu AK,Eells JT,et al.Opioid- induced second window of cardioprotection:potential role of mitochondrial KATP channels[J].Circ Res,1999,84:846
[14]韦星,冯大明,刘德平.去甲肾上腺素预处理对大鼠缺血/再灌注心肌的延迟保护作用[J].衡阳医学院学报,2000,28(2):140
[15]Bolli.The late phase of preconditioning[J].Circ Res,2000,87:972
[16]Qiu Y,Ping P,Tang XL,et al.Directe vidence that protein kinase C plays an essential role in the development of late preconditioning against myocardia stunning in conscious rabbits and that epsilon is the isoform in volved[J].J Cli Invest,1998,101:2182
[17]Dawn B,Xuan YT,Qiu Y,etal.Bifunctional role of protein tyrosine kinases in late preconditioning against myocardial stunning in conscious rabbits[J].Circ Res,1999,85(12):1154
[18]董丰,龚开政,张振刚,等.PKC和ERK在大鼠心肌缺氧预处理延迟保护机制中的作用[J].中国病理生理杂志,2003,19(4):503
[19]Weinbrenner C,Nelles M,Herzog N,et al.Remot preconditioning by infrarenal occlusion of the aorta protect-the heart from infarction:a newly -identified non-neuronal but PKC-dependent pathway[J].Cardiovascular Research,2002,55(3):590
[20]Dawn B,Xuan YT,Qiu Y,et al.Bifunctional role of proteinty rosine kinases in late preconditioning against myocardial stunning in conscious rabbits[J].Cir Res,1999,85:1154
[21]Ping P,Mutphy E.Role of p38 mitogen-activated protein kinases in preconditioning a detrimental factor or protective kinase[J].Cire Res,2000,86:921
[22]Dana A,Skarli M,Paakrivopoulou J,et al.Adenosine Al receptor induced delayed preconditioning in rabbits:induction of p38 mitogen - activated protein kinase activation and HSP27 phosphory lation via a tyrosine kinase and protein kinase C - dependent mechanism[J]. Circ Res, 2000, 86: 989
[23] Noma A. ATP-regulated K~+ channels in cardiacmuscle[J].Nature, 1983, 305: 147
[24] Inoue I, Nagase H, Kishi K, et al. ATP-sensitive K~+ channel in the mitochondrial inner membrane[J]. Nature, 1991,352: 244
[25] Liu H, Chen H, Yang X, Cheng J. ATP sensitive K~+ channel may be involved in the protective effects of preconditioning in isolated guinea pig cardiomyocytes [J].Chin Med J(Engl), 2001, 114(2): 178
[26]Bernardo N L, D. Angelo M, Okubo S, et al.Delayed ischemic preconditioning imediated by opening of ATP-sensitive potassium channels in the rabbithear[J]. Am J Physiol, 1999, 276(4Pt2): 1323
[27] Takashi E,Wang Y,Ashraf M.Activation of mitochondrial K(ATP) channe elicits late preconditioning against myocardial in farction via protein kinase C signaling pathway[J]. Circ Res, 1999,85: 1146
[28] Kukreja R C. Role of K_(ATP) channel in heart and pharmacological preconditioning[J]. Ann N Y Acad Sci ,1999, 874: 211
[29] Zhao T C,Hines D S,Kukreja R C.Adenosine induced late preconditioning in the mouse hearts: Role p38MAP kinase and mitochondrial K_(ATP) channels[J].Am J Physiol, 2001, 280: 1278
[30] Takano H, Bolli R, Black R G, et al. A1 or A3 receptors induce late preconditioning against infarction in conscious rabbits by different mechanisms[J]. Cir Res, 2001,88:520
[31] Schultz JJ, Hsu A K, Nagase H, et al. TAN-67, a deltal-opioid receptor agonist, reduces infarct size via activity of Gi/o protein and K_(ATP) channels [J]. Am J Physiol, 1998, 274 (3pt2): 909
[32] Zhao TC, Hines DS, Kukreja RC. Adenosine-induced late preconditioning in mouse hearts: role of p38 MAP kinase and mitochondrial KATP channels[J]. Am J Physiol Heart Circ Physiol, 2001, 280: 1278
[33] Fryer RM, Hsu AK, Eel Is JT, et al. Opioid-induced second window of cardioprotection potential role of mitochondrial K_(ATP) channels[J]. Circ Res, 1999, 84:846
[34] Ockaili R,Emani VR,Okubo S, et al. Opening of mitochondrial KATP channe induces early and delayed cardioprotective effect: role of nitric oxide[J].Am Physiol. 1999, 277 (6Pt2):H2425
[35] Joyeux M,Bouchard JF,Lamontagne D,et al.Heart stress -induced protection of endothelial function against is chaemic injury is abolished by ATP - sensitive potassium channel blockade in the isolated rat heart[J].Br J Pharmacol, 2000, 130:345
[36] Liana BT.Direct preconditioning of cardiac ventricular myocytes via adenosine Al receptor end KATP channel[J].Am J physiol, 1996, 271(SPt2):1769
[37] Cleveland JC Jr, Meldrvm DR, Rowland RT,et al. Adenosine preconditioning of human myocardium is dependent upon theATP-sensitive K~+ channel [J]. J Mol Cell Cardiol, 1997,29(1): 175
[38] Jiang BT. Protein kinase C-mediated preconditioning of cardiac myocytes: role of adenosine receptor and K_(ATP) channel[J]. Am J Physiol, 1997, 273(2pt2):847
[39] Zhuang JG, Zhang Y, Zhou ZN. Hypoxic preconditioning upregulates KATPchannels through activation of protein kinase C in rat ventricular myocytes[J].ACTAPHARMACOLOGICA SINICA, 2000, 21 (9): 845
[40] Wang Y, Hirai K, Ashraf M. Activation of mitochondrial ATP-sensitive K~+ channel for cardiac protection against ischemic injury is dependent on protein kinase Cactivity [J]. Circ Res, 1999, 85:731
[41] Fryer RM, Eells JT, Hsu AK, et al . Ischemic preconditioning in rats: role of mitochondrial K_(ATP) channel in preservation of mitochondrial function[J]. Am J Physiol Heart Circ Physiol, 2000, 278:305
[42] Brain. Myocardial K_(ATP) channels in preconditioning[J]. Circ Res, 2000, 87:845
[43] Korge P,Honda HM,Weiss JN.Protection of cardiac mitochondria by diazoxide and protein kinase C: implications for ischemic preconditioning [J]. Proc Natl Acad Sci USA, 2002,99: 3122
[44] de Klaver MJM, Manning L, Palmer LA et al. Isaflurane Pretreatment Inhibits Cytokine— induced Cell Death in Cultured Rat Smooth Muscle Cells and Human Endothelial Cells [J]. Anesthesiology, 2002, 97:24
[45] Beresewicz A, Maczewski M, Duda M. Effect of classic preconditioning and diazoxide on endothelial function and O~(2-) and NO generation in the post-ischemic guinea-pig heart[J].Cardiovascular Research, 2004, 63:—118
[46] Maczewski M, Duda M, Pawlak W, et al. Endothelial protection from reperfusion injury by ischemic preconditioning and diazoxide involves a SOD-like anti-02-mechanism[J]. J Physiol Pharmacol, 2004, 55:537
[47] Toyoda Y, Friehs I, Parker RA, et al. Differential role of sarcolemmal and mitochondrial K_(ATP) channels in adenosine enhanced ischemia preconditioning[J]. Am J Phys Circ Physiol, 2000, 279:2694
[48] Pain T, Yang XM, Stuart D, et al. Opening mitochondrial K_(ATP) channel triggers the perconditioned state by generating free radicals[J]. Circ Res, 2000, 87:460
[49] Stowe DF, Kevin LG. Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics[J]. Antioxid Redox Signal,2004, 6:439
[50] Vanden Hoek TL, Becker LB, Shao Z, et al . Reactive oxygen species released from mitochondria during brief hypoxia induce preconditioning in cardiomyocytes [J]. J Biol Chem, 1998, 273: 18092
[51]Murata M,Akao M,O.Rourke B,et al.Mitochondrial ATP-sensitive potassium channels attenuate matrix Ca~(2+)over load during simulated ischemia and reperfusion:possible mechanism of cardioprotection[J].CircRes,2001,89:891
[52]Cuevas P,Carceller F,Martinez-CosoV,et al.Fibroblast growth factor cardioprotection against ischemia-reperfusion injury may involve K~+ ATP channels[J].Eur J Med Res,2000,5:145
[53]Latchman DS.Heat shock proteins and cardiacprotection[J].Cardiovasc Res,2001,51(4):637
[54]Marber MS,Mestril R,Chi S-H,et al.Over expression of the rat inducible 70-kDa heat stress protein in transgenic mouse increases the resistance o fthe heart to ischemic injury[J].J Clin Invest,1995,95(4):1446
[55]Latchman DS.Heat shock protein and cadiac protection[J].Cardiovasc-Res.2001.51(4):637
[56]Zhou JJ,Pei JM,Wang GY.Inducible HSP70 mediates delayed cardio-protection via U-5048H pretreatment in rat ventricular myocytes[J].Am-J-Physiol-Heart-Cire-Physiol,2001,281(1):40
[57]傅俊英.心肌预适应延迟保护的研究现状及应用前景[J].心血管病学进展,2004,24(2):92
[58]Dana A,Jonassen AK,Yamashita N,et al.Adenosine Al receptor activation induces delayed preconditioning in rats mediated by manganese superoxide dismutase[J]. Circulation,2000,101: 2841
[59] Zhao T, Xi L, Chel 1 iah J,et al. Inducible nitric oxide synthase mediates delaye myocardial protection induced by activation of adenosine Al receptors: evidence from gene - knockout mice[J]. Circulation, 2000,102:902
[60] Xuan YT,Tang XL, Baner jee S, et al. Nuclear factor-kappaB plays an essential role in the late phase of ischemic preconditioning in conscious rabbits[J].CircRes, 1999, 84: 1095
[2]朱方.缺血预处理保护心肌作用的分子生物学机制[J].心血管病学进展,1998,19(4):214
[3]梁日欣,廖福龙,韩东.川芎嗪预处理对清醒大鼠心肌缺血再灌注损伤的保护作用[J].中国实验方剂学杂志,2002,8(1):21
[4]陈锋,王成天,王焱林,等.三七总皂苷预处理对在体大鼠心肌缺血再灌注的保护作用[J].中华麻醉学杂志,2000,20(7):437
[5]张卫军,史载祥,王蓓蓓,等.大蒜素模拟心肌缺血预处理作用的研究[J].中国循环杂志,2000,15(3):140
[6]程桂荣,易胜中.黄芪预处理大鼠心肌保护效应的实验研究[J].高血压杂志,2001,9(4):326
[7]卫洪昌,王秀薇,吕嵘,等.益心口服液药物预处理对大鼠心肌缺血再灌注损伤的影响[J].药学实践杂志,2001,9(3):157
[8]黄政德,张玉生,葛金文.加味丹参饮对家兔动脉粥样硬化形成影响的研究[J].湖南中医学院学报.2002,22(4):4
[9]黄政德,葛金文,张玉生.加味丹参饮对家兔缺血再灌注损伤心肌延迟保护作用的研究[J].湖南中医杂志,2003,19(6):52
[10]徐叔云,卞如濂.药理实验方法学[M].第2版.北京:人民卫生出版社,2002,45.
[11]刘建文.药理实验方法学-新技术与新方法[M].北京:化学工业 出版社,2003.258
[12]潘启超,胥彬.肿瘤药理学与化学治疗学[M].郑州:河南医科大学出版社,2000.783.
[13]黄世敬,翁维良.冠心病辨证诊断规范化研究概况[J].辽宁中医杂志,2000,27(3):142
[14]朱明军,王永霞.CHD中医辨证研究进展[J].上海中医药大学学报,2006,20(1):72
[15]陈贵延,薛赛琴.最新国内外疾病诊疗标准[S].北京:学苑出版社,1992.209-212,678
[16]中西医结合心血管学会.CHD的中医辨证标准[S].中西医结合杂志,1991,11(5):257
[17]中华人民共和国卫生部.中药新药治疗胸痹心痛的临床研究指导原则[S].1993.41
[18]郑筱萸.中药新药临床研究指导原则[S].北京:中国医药科技出版社,2002
[19]王永炎.中医内科学[M].上海:上海科学技术出版社,1997
[20]陈可冀,张之南,梁子钧,等.血瘀证与活血化瘀研究[M].上海:上海科学技术出版社,1990.127-137
[21]刘德恒,许真真,郭伟聪.CHD心绞痛395例中医证型特点探讨[J].中医杂志,1995,35(1a):517
[22]郭志华.CHD心绞痛2432例中医辨证分型综合统计分析[J].湖南中医杂志,1998,14(2):7
[23]张秋雁,邓冰湘.CHD心绞痛临床中医证型分布的回顾性分析[J].中医研究,2005,18(11):23
[24]旷惠桃,潘远根.CHD心绞痛临床证型分类探讨[J].中医杂志,1997,38(12):742
[25]胡冬裴.胸痹证治文献研究[J].山东中医药大学学报,2005,29(1):37
[26]马晓昌,尹太英,陈可冀,等.CHD中医辨证分型与冠状动脉造影所见相关性比较研究[J].中国中西医结合杂志,2001,21(9):654
[27]张敏州,丁邦晗,张维东,等.375例胸痹心痛患者冠状动脉造影结果与中医证型的对比研究[J].中国中西医结合急救杂志,2004,11(2):115
[28]李俊,李小敏,刘映峰.冠脉狭窄程度与血脂脂蛋白及中医证型关系[J].辽宁中医杂志,1999,26(11):486
[29]赵亚莉,杨幼新.CHD心电图与中医辨证分型的关系[J].江苏中医,2001,22(9):20
[30]岑永庄,黎学松.CHD常见心律失常与中医辨证分型关系的临床研究[J].新中医,1998,30(8):34
[31]周中山.CHD心绞痛中医证型与血液流变学的相关性研究[J].湖南中医药导报,2001,7(7):360
[32]丘瑞香,罗致强.CHD血瘀证血液理化特性与中医证型相关性研究[J].中医杂志,2002,43(5):378
[33]吕芳芳,黄文.CHD心绞痛不同证型与血液流变关系的探讨[J].北京中医,2004,23(6):327
[34]蔡辉,宁静,吴利群,等.血瘀证患者甲皱微循环检测的研究[J].中国医药学报,1995,10(3):30
[35]张三林,赵京生,张海涛,等.CHD患者中医证型与甲襞微循环变化的相关性研究[J].微循环学杂志,1999,9(2):46
[36]梁东辉,尹炳生,曾昭龙,等.老年CHD痰瘀辨证与血清脂蛋白谱检测的探讨[J].中国中西医结合杂志,1999,1(3):155
[37]庄德成,朱学云,钱小奇,等.高脂血症辨证分型与血脂指标的相关性研究[J].江苏中医,2001,22(9):18
[38]袁肇凯,简亚平,黄献平,等.高脂血症痰瘀辨证的血脂和血流动力学检测分析[J].湖南中医学院学报,2001,21(3):1
[39]毛成,叶式,刘强,等.CHD中医辨证分型与胰岛素抵抗关系的初步研究[J].中国中西医结合杂志,2001,21(9):657
[40]孙锡印,杨突琳.CHD气滞血瘀与气虚血瘀型间血载脂蛋白的异同及辨治影响[J].江苏中医,1997,18(6):40
[41]张月愁,梁东辉,李小敏,等.CHD疾病辨证分型与血清血脂蛋白平衡失调的研究[J].中国中西医结合杂志,1995,15(1):9
[42]张憋,梁东辉,曾昭龙,等.CHD痰瘀辨证与血清血脂蛋白谱检测的探讨[J].中国中西医结合杂志,1999,19(3):155
[43]蔡钦朝,汪琼华,吴云智,等.血瘀证患者血管内皮内分泌功能的观察[J].安徽中医学院学报,1998,17(2):61
[44]陈云波,侯孟君,王奇,等.血瘀证兔血清对培养的血管内皮细胞活性因子基因表达的影响[J].广州中医药大学学报,2001,18(2):100
[45]刘红旭,黄丽娟,金欢.血瘀胸痹血浆内皮源性收缩/舒张因子水平及治疗影响研究[J].北京中医,1995,(6):49
[46]陈建鸿,杜建.CHD中医辨证与内皮素及降钙素基因相关肽关系的临床研究[J].中医杂志,1998,39(2):108
[47]秦鉴,金明华,邓江华,等.化湿和化瘀法治疗CHD的临床研究[J].中国中西医结合杂志,1997,17(9):519
[48]过鑫昌,丁怀翌,戚文航,等.前列腺素、血小板功能CHD中医辨证分型与蛋白C抗原的关系[J].中国中西医结合杂志,1991,11(5):263
[49]梁铁军,高顺宗,张发丽,等.CHD患者抗凝系统改变与中医证型关系[J].中国中西医结合杂志,1995,15(10):599
[50]骆丽娟.CHD证型与P-选择素、TXB2及6-Keto-PGF含量变化关系的研究[J].上海中医药杂志,2002,36(7):13
[51]吕中,祝光礼,施赛珠.CHD患者单核细胞凝血/纤溶活性改变与证型关系[J].浙江中医杂志,2002,37(1):33
[52]梁晓春,郭赛珊.前列腺素与中医中药[J].中西医结合杂志,1990,10(3):185
[53]严卉,胡晓晟,陈君柱,等.血浆同型半胱氨酸和冠状动脉粥样硬化严重程度与中医证型的关系[J].中国中西医结合杂志,2002,22(11):813
[54]中国医学科学院阜外医院等.冠心Ⅱ号治疗CHD心绞痛164例远期疗效观察[J].心血管疾病,1978,(1):22
[55]陈可冀,钱振淮,张问渠,等.精制冠心片双盲法治疗CHD心绞痛112例疗效分析[J].中华心血管杂志,1982,(2):85
[56]周小青,罗尧岳,谢小兵,等.五首活血化瘀方对实验性动脉粥样硬化家兔血脂、载脂蛋白的影响[J].中国中医药信息杂志,2003,10(4):29
[57]王瑷芬,翟雯娟.红花注射液治疗CHD心绞痛、心肌缺血临床观察[J].医学理论与实践,2003,16(9):1002
[58]高承贤,丁志山,沃兴德,等.血府逐瘀汤抗心肌缺血及耐缺氧作用的实验研究[J].浙江中医学院学报,2001,25(2):45
[59]余追,欧阳静萍,刘永明,等.当归抗家兔主动脉粥样硬化形成的作用[J].中国动脉硬化杂志,2000,8(1):46
[60]李鲁杨,任国华,刘向红,等.扶正降黏胶囊改善CHD患者血 栓前期相关因素的临床研究[J].中国中西医结合杂志,2005,25(8):691
[61]谢建安,刘新红.心血丹注射液治疗CHD患者的疗效及其对血液流变学的影响[J].陕西中医,2005,26(10):1064
[62]朱薇,贾满仓.复方丹参滴丸治疗CHD心绞痛60例临床观察[J].中国中医急症,2005,14(8):742
[63]杨永华,朱伟荣,朱建秀,等.灯盏花素治疗CHD30例临床研究[J].中西医心脑血管病杂志,2003,1(3):141
[64]黄志平,李小林,廖庆文,等.川芎嗪对CHD患者抗氧化酶、脂质过氧化物及脂肪酸含量的影响[J].中国中医药科技,2005,12(5):272
[65]赵泽红,郑祖云,范邻翔,等.补心活络胶囊对CHD及其脂质过氧化作用的影响[J].广州中医药大学学报,2002,6(2):85
[66]王昕.归芪胶囊对家兔心肌缺血-再灌注损伤中SOD,MDA,NOS 影响实验研究[J].中医药学刊,2004,22(10):1815
[67]丘瑞香,贺敬波,蓝军,等.心脉通胶囊保护血管内皮细胞损伤的临床研究[J].中国中西医结合杂志,1998,18(2):74
[68]丘瑞香,贺敬波,蓝军,等.心脉通胶囊对CHD患者心肌缺血总负荷影响及其作用机制探讨[J].中国中西医结合杂志,2000,20(1):19
[69]丘瑞香,祁翠仪,贺敬波,等.心脉通胶囊对CHD患者血管活性因子的调节作用[J].中国医药学报,1999,14(1):29
[70]汪坚敏,王俏,朱健.三七总皂苷对CHD不稳定型心绞痛内皮功能的影响[J].临床中老年保健,2002,5(3):183
[71]华宇明,管耘园,金恒,等.复方丹参对血浆内皮素和一氧化氮浓度的影响[J].中国临床药理学与治疗学,2000,5(4): 363
[72]曹静.复脉灵颗粒治疗气滞血瘀型CHD心绞痛的临床研究[J].中西医结合心脑血管病杂志,2005,3(8):673
[73]杨庆福,李彩玲,陈俭.复方丹参滴丸对CHD心绞痛患者血管内皮功能的影响[J].新乡医学院学报,2003,20(2):127
[74]黎玉,万福生,李少华,等.川芎嗪对大鼠缺血心肌线粒体NO 及自由基的影响[J].中医药学报,2004,32(2):47
[75]谭元生,邓圣明,谭超.药物预处理对缺血再灌注损伤心肌的保护作用[J].中医药学刊,2003,21(6):877
[76]梁日欣,廖福龙,韩东.川芎嗪预处理对体外培养乳鼠心肌细胞低氧再给氧损伤的保护作用[J].中药药理与临床,2000,16(6):7
[77]傅俊英,史载祥,张久亮,等.大蒜素延迟预处理对实验性兔心肌梗死损伤保护作用的研究[J].中国比较医学杂志,2005,15(4):221
[78]郭利平,高秀梅,张萌.丹酚酸B预处理的心脏微血管内皮细胞延迟保护作用研究[J].天津中医,2002,19(1):41
[79]刘颖,陈晨,吴伟康,等.四逆汤预处理对大鼠心缺血再灌注后心功能的延迟保护作用[J].中药药理与临床,2006,22(1):11
[80]Qiu Y,Ping P,Tang XL,et al.Directe vidence that protein kinase C plays an essential role in the development of late preconditioning against myocardia stunning in conscious rabbits and that epsilon is the isoform in volved[J].J Cli Invest,1998,101:2182
[81]Dawn B,Xuan YT,Qiu Y,et al.Bifunctional role of protein tyrosine kinases in late preconditioning against myocardial stunning in conscious rabbits [J].Circ Res,1999,85(12): 1154
[82] Noma A.. ATP-regulated K~+ channels in cardiacmuscle [J].Nature, 1983, 305:147
[83] Inoue I, Nagase H, Kishi K, et al. ATP-sensitive K~+ channel in the mitochondrial inner membrane[J]. Nature, 1991,352:244
[84] Liu H, Chen H, Yang X, Cheng J. ATP sensitive K~+ channel may be involved in the protective effects of preconditioning in isolated guinea pig cardiomyocytes [J].Chin Med J(Engl), 2001, 114(2): 178
[85] Kukreja RC. Role of K_(ATP) channel in heart and pharmacological preconditioning[J]. Ann N Y Acad Sci, 1999, 874: 211-221.
[86] Zhao T C,Hines D S,Kukreja R C.Adenosine induced late preconditioning in the mouse hearts:Role p38MAP kinase and mitochondrial K_(ATP) channels [J]. Am J Physiol,2001, 280: 1278
[87] Takano H, Bolli R, Black R G, et al. Al or A3 receptors induce late preconditioning against infarction in conscious rabbits by different mechanisms [J]. Cir Res,2001,88:520
[88] Schultz JJ, Hsu A K, Nagase H, et al.TAN-67, a deltal-opioid receptor agonist, reduces infarct size via activity of Gi/o protein and K_(ATP) channels[J]. Am J Physiol, 1998,274 (3pt2): 909
[89] Zhao TC, Hines DS, Kukreja RC. Adenosine-induced late preconditioning in mouse hearts: role of p38 MAP kinase and mitochondrial KATP channels[J]. Am J Physiol Heart Circ Physiol, 2001, 280: 1278
[90] Fryer RM, Hsu AK, Eel Is JT, et al. Opioid-induced second window of cardioprotection potential role of mitochondrial K_(ATP) channels [J]. Circ Res, 1999, 84:846
[91] Liana BT.Direct preconditioning of cardiac ventricular myocytes via adenosine Al receptor end KATP channel[J].Am J physiol. 1996 Nov;271 (SPt2): 1769
[92] Cleveland JC Jr, Meldrvm DR, Rowland RT,et al.Adenosine preconditioning of human myocardium is dependent upon theATP-sensitive K~+ channel[J].J Mol Cell Cardiol, 1997,29(1): 175
[93] Jiang BT. Protein kinase C-mediated preconditioning of cardiac myocytes: role of adenosine receptor and K_(ATP) channel[J]. Am J Physiol, 1997, 273 (2pt2): 847
[94] Zhuang JG, Zhang Y, Zhou ZN. Hypoxic preconditioning upregulates KATPchannels through activation of protein kinase C in rat ventricular myocytes[J].ACTAPHARMACOLOGICA SINICA, 2000, 21 (9): 845
[95] Wang Y, Hirai K, Ashraf M. Activation of mitochondrial ATP-sensitive K~+ channel for cardiac protection against ischemic injury is dependent on protein kinase Cactivity[J].Circ Res, 1999, 85: 731
[96] Fryer RM, Eells JT, Hsu AK, et al . Ischemic preconditioning in rats: role of mi tochondr ial K_(ATP) channel in preservation of mitochondrial function[J]. Am J Physiol Heart Circ Physiol, 2000, 278:305
[97] Brain. Myocardial KATP channels in preconditioning [J].Circ Res, 2000, 87:845
[98] Korge P,Honda HM,Weiss JN.Protection of cardiac mitochondria by diazoxide and protein kinase C: implications for ischemic precondi tioning [J]. Proc Natl Acad Sci USA, 2002, 99: 33122
[99] de Klaver MJM, Manning L, Palmer LA, et al. Isaflurane Pretreatment Inhibits Cytokine — induced Cell Death in Cultured Rat Smooth Muscle Cells and Human Endothelial Cells [J]. Anesthesiology, 2002, 97:24
[100] Beresewicz A, Maczewski M, Duda M. Effect of classic preconditioning and diazoxide on endothelial function and O~(2-) and NO generation in the post-ischemic guinea-pig heart[J]. Cardiovascular Research, 2004, 63: 118
[101] Maczewski M, Duda M, Pawlak W, et al. Endothelial protection from reperfusion injury by ischemic preconditioning and diazoxide involves a SOD—1 ike anti-02-mechanism[J]. J Physiol Pharmacol, 2004, 55:537
[102] Toyoda Y, Friehs I, Parker RA, et al. Differential role of sarcolemmal and mi tochondrial K_(ATP) channels in adenosine enhanced ischemia preconditioning[J]. Am J Phys Circ Physiol, 2000, 279:2694
[103] Pain T, Yang XM, Stuart D, et al. Opening mi tochondrial K_(ATP) channel triggers the percondit ioned state by generating free radicals[J]. Circ Res, 2000, 87:460-466
[104] Stowe DF, Kevin LG. Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics[J]. Antioxid Redox Signal,2004, 6:439
[105] Vanden Hoek TL, Becker LB, Shao Z, et al . Reactive oxygen species released from mitochondria during brief hypoxia induce preconditioning in cardiomyocytes[J]. J Biol Chem, 1998, 273: 18092
[106] Murata M, Akao M, O. Rourke B , et al. Mitochondrial ATP-sensitive potassium channels attenuate matrix Ca~(2+) over load during simulated ischemia and reperfusion: possible mechanism of cardioprotection[J]. CircRes, 2001, 89: 891
[107] Cuevas P,Carceller F,Martinez-CosoV, et al.Fibroblast growth factor cardioprotection against ischemia-reperfusion injury may involve K~+ ATP channels[J].Eur J Med Res, 2000, 5: 145
[108] Polakowski JS, Wegner CD, Cox BF. Bimoclomol elevates heat Shock protein 70 and cytoprotects rat neonatal cardiomyocytes. Eur J Pharmacol, 2002, 435(1): 73
[109] Yellen DM. Baxter GF. A "second window of protection" or delayed preconditioning phenomenon: future horizons for myocardial protection[J]? J Mol Cell Cardiol,1995,27: 1023
[110] Yamashita N, Nishida M, Hoshida S, et al. Induction of manganese superoxide dismutation in rat cardiac myocytes increase tolerance to hypoxia 24 hours after precondioning[J].J Clin lovest,1994,94:2193
[111]刘秀华,陈奎,武旭东,等.缺血预处理的普遍性[J].北京医科大学学报,1996,28:170
[112]Zhou X,Zhai X.Astral M.Direct evidence that initial oxidative stress triggered by preconditioning contributes to second window of protection by endogenous antioxidant enzyme in myocytes[J].Circulation,1996,93:1177
[113]Latchman DS.Heat shock proteins and cardiacpro-tection [J].Cardiovasc Res,2001,51(4):637-646
[114]Craig EA,Weissman IS.Homich AL.Heat shock protein and molecular chaperones:mediators of protein conformation and turnover in the cell[J].Cell,1994,78:491
[115]Marber MS,Mestril R,Chi S-H,et al.Over expression of the rat inducible 70-kDa heat stress protein in transgenic mouse increases the resistance of the heart to ischemic injury[J].J Clin Invest,1995,95(4):1446
[116]Latchman DS.Heat shock protein and cadiac protection[J].Cardiovasc-Res[J].2001,51(4):637
[117]Engel man DT,Chen CZ,Watanabe M,et al.Improved 4-and 6-hour myocardial preservation by hypoxic preconditioning[J].Circulation.1995,92(9Suppl):417
[118]Knowltor AA,Bercher P,Apstein CS.Rapid expression of heat shock protein in the rabbit after brief cardiac ischemia[J]. 7 Clin Invest. 1991,-87: 139
[119] Marber MS, Latchman DS, Walker JM, et al. Cardiac stress protein elevation 24 hour s after brief ischemia or heart stress is associated with resistance to myocardial infarction[J]. Circulation, 1993, 89:1264
[120] Zhou JJ, Pei JM, Wang GY. Inducible HSP70 mediates delayed cardio-protection via U-5048H pretreatment in rat ventricular myocytes[J].AmJ Physiol Heart Cire Physiol,2001, 281(1): 40
[1]金惠铭,卢建,殷莲华.细胞分子病理生理学[M].郑州:郑州大学出版社,2002.565
[2]Kudo M,Wang YG,Xu MF,et al.A denosine A(1) receptor mediates late preconditioning via activation of PKC-delta signaling pathway[J].Am J Physiol Heart Cire Physiol,2002,283(1):296
[3]DanaA,BaxterGF,WalkerJM,et al.Prolonging the delayed phase of myocardial protection:repetitive adenosine Al receptor activation maintains rabbit myocardium in a preconditioning statec[J].J Am Coll Cardiol,1998,31:1142
[4]Bolli R,Bhatti ZA,Tang XL,et al.Evidence that late preconditioning against myocardial stunning in conscious rabbits is triggered by the generation of nitric oxide[J].Circ Res,1997,81:42
[5]Banerjee S,Tang XL,Qiu Y.Nitroglycerin induces late preconditioning against myocardial stunning via a PKC-dependent path way[J].Am J Physiol Heart Circ Physiol,1997,81:2488
[6]Imagawa J,Yellon DM,Baxter GF.Pharmacological evidence that inducible nitric oxide synthesis is a mediator of delayed preconditioning[J].Br J Pharmacol,1999,126:701
[7]Sasaki N,Sato T,Ohler A,et al.Activation of mitochondrial ATP-dependent potassium channels by nitric oxide[J].Circulation,2000,101:439
[8]Shinmura K,Tang XL,Takano H,et al.Nitric oxide donors attenuate myocardial stunning in conscious rabbits[J].Am J Physiol,1999,277(6Pt2):H2495
[9]Takano H,Tang XL,Qiu Y,et al.Nitric oxide donors induce late preconditioning against myocardial stunning and infarction in conscious rabbits via an antioxidant-sensitive mechanism[J].Cire Res,1998,83:73
[10]Zhou FW,Li YJ,Deng HW.Early and delayed protection by capsaicinagains reperfusion in jury in rat heart[J].Acta Pharmacol Sin,1999,20:912
[11]Song QJ,Li.YJ,Deng HW.Early and delayed cardioprotection by heat stress is mediated by calcitonin gene-related peptide[J].Naunyn Schmiedebergs Arch Pharmacol,1999,359:477
[12]Peart JN,Gross GJ.Chronic exposure to morphine produces a marked cardioprotective phenotype in aged mouse hearts[J].Exp Gerontol,2004,39(7):1021
[13]Fryer RM,Hsu AK,Eells JT,et al.Opioid- induced second window of cardioprotection:potential role of mitochondrial KATP channels[J].Circ Res,1999,84:846
[14]韦星,冯大明,刘德平.去甲肾上腺素预处理对大鼠缺血/再灌注心肌的延迟保护作用[J].衡阳医学院学报,2000,28(2):140
[15]Bolli.The late phase of preconditioning[J].Circ Res,2000,87:972
[16]Qiu Y,Ping P,Tang XL,et al.Directe vidence that protein kinase C plays an essential role in the development of late preconditioning against myocardia stunning in conscious rabbits and that epsilon is the isoform in volved[J].J Cli Invest,1998,101:2182
[17]Dawn B,Xuan YT,Qiu Y,etal.Bifunctional role of protein tyrosine kinases in late preconditioning against myocardial stunning in conscious rabbits[J].Circ Res,1999,85(12):1154
[18]董丰,龚开政,张振刚,等.PKC和ERK在大鼠心肌缺氧预处理延迟保护机制中的作用[J].中国病理生理杂志,2003,19(4):503
[19]Weinbrenner C,Nelles M,Herzog N,et al.Remot preconditioning by infrarenal occlusion of the aorta protect-the heart from infarction:a newly -identified non-neuronal but PKC-dependent pathway[J].Cardiovascular Research,2002,55(3):590
[20]Dawn B,Xuan YT,Qiu Y,et al.Bifunctional role of proteinty rosine kinases in late preconditioning against myocardial stunning in conscious rabbits[J].Cir Res,1999,85:1154
[21]Ping P,Mutphy E.Role of p38 mitogen-activated protein kinases in preconditioning a detrimental factor or protective kinase[J].Cire Res,2000,86:921
[22]Dana A,Skarli M,Paakrivopoulou J,et al.Adenosine Al receptor induced delayed preconditioning in rabbits:induction of p38 mitogen - activated protein kinase activation and HSP27 phosphory lation via a tyrosine kinase and protein kinase C - dependent mechanism[J]. Circ Res, 2000, 86: 989
[23] Noma A. ATP-regulated K~+ channels in cardiacmuscle[J].Nature, 1983, 305: 147
[24] Inoue I, Nagase H, Kishi K, et al. ATP-sensitive K~+ channel in the mitochondrial inner membrane[J]. Nature, 1991,352: 244
[25] Liu H, Chen H, Yang X, Cheng J. ATP sensitive K~+ channel may be involved in the protective effects of preconditioning in isolated guinea pig cardiomyocytes [J].Chin Med J(Engl), 2001, 114(2): 178
[26]Bernardo N L, D. Angelo M, Okubo S, et al.Delayed ischemic preconditioning imediated by opening of ATP-sensitive potassium channels in the rabbithear[J]. Am J Physiol, 1999, 276(4Pt2): 1323
[27] Takashi E,Wang Y,Ashraf M.Activation of mitochondrial K(ATP) channe elicits late preconditioning against myocardial in farction via protein kinase C signaling pathway[J]. Circ Res, 1999,85: 1146
[28] Kukreja R C. Role of K_(ATP) channel in heart and pharmacological preconditioning[J]. Ann N Y Acad Sci ,1999, 874: 211
[29] Zhao T C,Hines D S,Kukreja R C.Adenosine induced late preconditioning in the mouse hearts: Role p38MAP kinase and mitochondrial K_(ATP) channels[J].Am J Physiol, 2001, 280: 1278
[30] Takano H, Bolli R, Black R G, et al. A1 or A3 receptors induce late preconditioning against infarction in conscious rabbits by different mechanisms[J]. Cir Res, 2001,88:520
[31] Schultz JJ, Hsu A K, Nagase H, et al. TAN-67, a deltal-opioid receptor agonist, reduces infarct size via activity of Gi/o protein and K_(ATP) channels [J]. Am J Physiol, 1998, 274 (3pt2): 909
[32] Zhao TC, Hines DS, Kukreja RC. Adenosine-induced late preconditioning in mouse hearts: role of p38 MAP kinase and mitochondrial KATP channels[J]. Am J Physiol Heart Circ Physiol, 2001, 280: 1278
[33] Fryer RM, Hsu AK, Eel Is JT, et al. Opioid-induced second window of cardioprotection potential role of mitochondrial K_(ATP) channels[J]. Circ Res, 1999, 84:846
[34] Ockaili R,Emani VR,Okubo S, et al. Opening of mitochondrial KATP channe induces early and delayed cardioprotective effect: role of nitric oxide[J].Am Physiol. 1999, 277 (6Pt2):H2425
[35] Joyeux M,Bouchard JF,Lamontagne D,et al.Heart stress -induced protection of endothelial function against is chaemic injury is abolished by ATP - sensitive potassium channel blockade in the isolated rat heart[J].Br J Pharmacol, 2000, 130:345
[36] Liana BT.Direct preconditioning of cardiac ventricular myocytes via adenosine Al receptor end KATP channel[J].Am J physiol, 1996, 271(SPt2):1769
[37] Cleveland JC Jr, Meldrvm DR, Rowland RT,et al. Adenosine preconditioning of human myocardium is dependent upon theATP-sensitive K~+ channel [J]. J Mol Cell Cardiol, 1997,29(1): 175
[38] Jiang BT. Protein kinase C-mediated preconditioning of cardiac myocytes: role of adenosine receptor and K_(ATP) channel[J]. Am J Physiol, 1997, 273(2pt2):847
[39] Zhuang JG, Zhang Y, Zhou ZN. Hypoxic preconditioning upregulates KATPchannels through activation of protein kinase C in rat ventricular myocytes[J].ACTAPHARMACOLOGICA SINICA, 2000, 21 (9): 845
[40] Wang Y, Hirai K, Ashraf M. Activation of mitochondrial ATP-sensitive K~+ channel for cardiac protection against ischemic injury is dependent on protein kinase Cactivity [J]. Circ Res, 1999, 85:731
[41] Fryer RM, Eells JT, Hsu AK, et al . Ischemic preconditioning in rats: role of mitochondrial K_(ATP) channel in preservation of mitochondrial function[J]. Am J Physiol Heart Circ Physiol, 2000, 278:305
[42] Brain. Myocardial K_(ATP) channels in preconditioning[J]. Circ Res, 2000, 87:845
[43] Korge P,Honda HM,Weiss JN.Protection of cardiac mitochondria by diazoxide and protein kinase C: implications for ischemic preconditioning [J]. Proc Natl Acad Sci USA, 2002,99: 3122
[44] de Klaver MJM, Manning L, Palmer LA et al. Isaflurane Pretreatment Inhibits Cytokine— induced Cell Death in Cultured Rat Smooth Muscle Cells and Human Endothelial Cells [J]. Anesthesiology, 2002, 97:24
[45] Beresewicz A, Maczewski M, Duda M. Effect of classic preconditioning and diazoxide on endothelial function and O~(2-) and NO generation in the post-ischemic guinea-pig heart[J].Cardiovascular Research, 2004, 63:—118
[46] Maczewski M, Duda M, Pawlak W, et al. Endothelial protection from reperfusion injury by ischemic preconditioning and diazoxide involves a SOD-like anti-02-mechanism[J]. J Physiol Pharmacol, 2004, 55:537
[47] Toyoda Y, Friehs I, Parker RA, et al. Differential role of sarcolemmal and mitochondrial K_(ATP) channels in adenosine enhanced ischemia preconditioning[J]. Am J Phys Circ Physiol, 2000, 279:2694
[48] Pain T, Yang XM, Stuart D, et al. Opening mitochondrial K_(ATP) channel triggers the perconditioned state by generating free radicals[J]. Circ Res, 2000, 87:460
[49] Stowe DF, Kevin LG. Cardiac preconditioning by volatile anesthetic agents: a defining role for altered mitochondrial bioenergetics[J]. Antioxid Redox Signal,2004, 6:439
[50] Vanden Hoek TL, Becker LB, Shao Z, et al . Reactive oxygen species released from mitochondria during brief hypoxia induce preconditioning in cardiomyocytes [J]. J Biol Chem, 1998, 273: 18092
[51]Murata M,Akao M,O.Rourke B,et al.Mitochondrial ATP-sensitive potassium channels attenuate matrix Ca~(2+)over load during simulated ischemia and reperfusion:possible mechanism of cardioprotection[J].CircRes,2001,89:891
[52]Cuevas P,Carceller F,Martinez-CosoV,et al.Fibroblast growth factor cardioprotection against ischemia-reperfusion injury may involve K~+ ATP channels[J].Eur J Med Res,2000,5:145
[53]Latchman DS.Heat shock proteins and cardiacprotection[J].Cardiovasc Res,2001,51(4):637
[54]Marber MS,Mestril R,Chi S-H,et al.Over expression of the rat inducible 70-kDa heat stress protein in transgenic mouse increases the resistance o fthe heart to ischemic injury[J].J Clin Invest,1995,95(4):1446
[55]Latchman DS.Heat shock protein and cadiac protection[J].Cardiovasc-Res.2001.51(4):637
[56]Zhou JJ,Pei JM,Wang GY.Inducible HSP70 mediates delayed cardio-protection via U-5048H pretreatment in rat ventricular myocytes[J].Am-J-Physiol-Heart-Cire-Physiol,2001,281(1):40
[57]傅俊英.心肌预适应延迟保护的研究现状及应用前景[J].心血管病学进展,2004,24(2):92
[58]Dana A,Jonassen AK,Yamashita N,et al.Adenosine Al receptor activation induces delayed preconditioning in rats mediated by manganese superoxide dismutase[J]. Circulation,2000,101: 2841
[59] Zhao T, Xi L, Chel 1 iah J,et al. Inducible nitric oxide synthase mediates delaye myocardial protection induced by activation of adenosine Al receptors: evidence from gene - knockout mice[J]. Circulation, 2000,102:902
[60] Xuan YT,Tang XL, Baner jee S, et al. Nuclear factor-kappaB plays an essential role in the late phase of ischemic preconditioning in conscious rabbits[J].CircRes, 1999, 84: 1095