七氟醚后处理对室间隔缺损修补术患儿心肌缺血再灌注损伤的影响
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摘要
目的：
预处理和后处理都具有减轻心肌缺血／再灌注损伤、保护心肌的作用,但预处理必须在心肌缺血发生之前实施,显然限制了其在临床上的应用范围。七氟醚后处理可产生类似缺血后处理的效应,减轻心肌缺血再灌注损伤。七氟醚为目前临床麻醉中常用的吸入性全身麻醉药,近年来其心肌保护作用备受关注和研究。MDA的含量可反映机体内脂质过氧化的程度而间接反映细胞受氧自由基攻击的严重程度；SOD活性的高低反映机体清除氧自由基的能力；CK-MB曾经是诊断心肌损伤特别是心肌梗死的“金标准”；cTnI对检测心肌损伤最具有敏感性和特异性,是现今诊断和预测心肌损伤的最佳指标。本研究通过观察室间隔缺损修补术患儿围术期血清磷酸肌酸激酶同工酶(CK-MB)、心肌钙蛋白(cTnI)、丙二醛(MDA)和超氧化物歧化酶(SOD)的变化,探讨七氟醚后处理对室间隔缺损修补术患儿围术期心肌缺血再灌注损伤的影响及其机制。
方法：
32例(男18例,女14例)行室间隔缺损修补术的患儿,随机分为两组,实验组和对照组,每组各16例。实验组即七氟醚后处理组,主动脉开放前3 min开始小潮气量通气,同时吸入2.0vol%七氟醚,持续至主动脉开放后10min；而对照组在此期间未予七氟醚吸入。并分别于麻醉诱导前(T1)、主动脉阻断前即刻(T2)、主动脉开放前即刻(T3)、主动脉开放后5min(T4)、主动脉开放后10min(T5)以及主动脉开放后30min(T6)共6个时间点采中心静脉血,提取上清置于EP管-20℃保存,检测血清磷酸肌酸激酶同工酶(CK-MB)、心肌钙蛋白(cTnI)、丙二醛(MDA)和超氧化物歧化酶(SOD)浓度。并于上述6个时间点记录HR、MAP以及CVP。
结果：
两组患儿术前、术中及术后的血流动力学指标均保持稳定。
两组患儿再灌注后各个时段血清CK-MB水平均较术前高(p<0.05或0.01),但与对照组比较,七氟醚后处理组则降低(p<0.05)。两组患儿再灌注后各个时段血清cTnI水平均较术前高(p<0.01),但与对照组比较,七氟醚后处理组则降低(p<0.05)。
七氟醚后处理组MDA浓度再灌注后与术前比较显著升高(p<0.05或0.01),但低于对照组(p<0.01)。同时,两组再灌注后血清SOD活性再灌注后与术前比较显著降低(p<0.05或0.01),七氟醚后处理组高于对照组(p<0.01)。
结论：
七氟醚后处理可减轻室间隔缺损修补术患儿围术期心肌缺血再灌注损伤,其机制可能与其抗氧化作用有关。
OBJECTIVES:
Both anesthetic preconditioning and postconditioning are promising therapeutic strategies of attaining protection against myocardial ischemia-reperfusion injury(MIRI). Clinically,anesthetic postconditioning administered right at the onset of reperfusion is more attractive than anesthetic preconditioning,in that interventions could be done at the time of reperfusion and do not have to predict an ischemic episode. Sevoflurane, a commonly used volatile anesthetic, has been demonstrated in clinical and experimental studies, to have protective profiles against MIRI. However, the underlying mechanism responsible for such cardioprotection induced by sevoflurane,particularly sevoflurane postconditioning, remains poorly understood. Therefore, this study was undertaken to probe into the effect of sevoflurane postconditioning on myocardial ischemia-reperfusion injury of children undergoing repair of interventricular septal defect through detecting the levels of CK-MB, cTnl, MDA and activity of SOD in human blood.
METHODS:
Thirty-two (18 male,14 female) children scheduled for elective repair of interventricular septal defect surgery with cardiopulmonary bypass were randomly divided into two groups of 16 children:sevoflurane postconditioning group and control group.In sevoflurane postconditioning group, low tidal volume ventilation was started at 3 min before declamping aorta and at the same time 2.0vol% sevoflurane was inhaled,which lasted to 10 min after declamping aorta. But during this period sevoflurane was not inhaled in control group. The central venous blood samples were collected for the measurements of creatine kinase(CK-MB), cTnI, superoxide dismutase(SOD) and malondialdehyde(MDA) before anesthesia (T1), immediately before clamping aorta(T2), immediately before declamping aorta(T3),5min after declamping aorta (T4), 10min after declamping aorta (T5) and 30min after declamping aorta(T6). HR, MAP and CVP were recorded at T1-T6 also.
RESULTS:
Hemodynamic parameters were kept stable throughout in both groups.
At each period of time after reperfussion, compared with T1, the contents of CK-MB in both groups increased significantly (p<0.05 or 0.01). But compared with control group,the content of CK-MB was significantly lower in SPC group(p<0.05). At each period of time after reperfussion,compared with Tl,the content of cTnl in both groups increased significantly (p<0.01). But compared with control group, the content of cTnl was significantly lower in SPC group(p<0.05).
The MDA in SPC group increased significantly (p<0.05 or 0.01)at T2-T6,compared with that at T1, but at T4-T6, the content of MDA in SPC group was significantly lower than that in control group(p<0.01). At T4-T6, the activity of SOD decreased(p<0.05 or 0.01) in both groups, and SOD in SPC group was higher than that in control group(p<0.01). It is suggested that sevoflurane postconditioning can inhibit increasing of MDA levels to attenuate myocardial ischemia/reperfusion injuries mediated by reactive oxygen series (ROS) during open-heart surgery.
CONCLUSION:
Sevoflurane postconditioning can attenuate myocardial ischeamia-reperfusion injury in children undergoing repair of interventricular septal defect surgery, and.the mechanisms are possiblely related to the antioxidant function of sevoflurane postconditioning.
预处理和后处理都具有减轻心肌缺血／再灌注损伤、保护心肌的作用,但预处理必须在心肌缺血发生之前实施,显然限制了其在临床上的应用范围。七氟醚后处理可产生类似缺血后处理的效应,减轻心肌缺血再灌注损伤。七氟醚为目前临床麻醉中常用的吸入性全身麻醉药,近年来其心肌保护作用备受关注和研究。MDA的含量可反映机体内脂质过氧化的程度而间接反映细胞受氧自由基攻击的严重程度；SOD活性的高低反映机体清除氧自由基的能力；CK-MB曾经是诊断心肌损伤特别是心肌梗死的“金标准”；cTnI对检测心肌损伤最具有敏感性和特异性,是现今诊断和预测心肌损伤的最佳指标。本研究通过观察室间隔缺损修补术患儿围术期血清磷酸肌酸激酶同工酶(CK-MB)、心肌钙蛋白(cTnI)、丙二醛(MDA)和超氧化物歧化酶(SOD)的变化,探讨七氟醚后处理对室间隔缺损修补术患儿围术期心肌缺血再灌注损伤的影响及其机制。
方法：
32例(男18例,女14例)行室间隔缺损修补术的患儿,随机分为两组,实验组和对照组,每组各16例。实验组即七氟醚后处理组,主动脉开放前3 min开始小潮气量通气,同时吸入2.0vol%七氟醚,持续至主动脉开放后10min；而对照组在此期间未予七氟醚吸入。并分别于麻醉诱导前(T1)、主动脉阻断前即刻(T2)、主动脉开放前即刻(T3)、主动脉开放后5min(T4)、主动脉开放后10min(T5)以及主动脉开放后30min(T6)共6个时间点采中心静脉血,提取上清置于EP管-20℃保存,检测血清磷酸肌酸激酶同工酶(CK-MB)、心肌钙蛋白(cTnI)、丙二醛(MDA)和超氧化物歧化酶(SOD)浓度。并于上述6个时间点记录HR、MAP以及CVP。
结果：
两组患儿术前、术中及术后的血流动力学指标均保持稳定。
两组患儿再灌注后各个时段血清CK-MB水平均较术前高(p<0.05或0.01),但与对照组比较,七氟醚后处理组则降低(p<0.05)。两组患儿再灌注后各个时段血清cTnI水平均较术前高(p<0.01),但与对照组比较,七氟醚后处理组则降低(p<0.05)。
七氟醚后处理组MDA浓度再灌注后与术前比较显著升高(p<0.05或0.01),但低于对照组(p<0.01)。同时,两组再灌注后血清SOD活性再灌注后与术前比较显著降低(p<0.05或0.01),七氟醚后处理组高于对照组(p<0.01)。
结论：
七氟醚后处理可减轻室间隔缺损修补术患儿围术期心肌缺血再灌注损伤,其机制可能与其抗氧化作用有关。
OBJECTIVES:
Both anesthetic preconditioning and postconditioning are promising therapeutic strategies of attaining protection against myocardial ischemia-reperfusion injury(MIRI). Clinically,anesthetic postconditioning administered right at the onset of reperfusion is more attractive than anesthetic preconditioning,in that interventions could be done at the time of reperfusion and do not have to predict an ischemic episode. Sevoflurane, a commonly used volatile anesthetic, has been demonstrated in clinical and experimental studies, to have protective profiles against MIRI. However, the underlying mechanism responsible for such cardioprotection induced by sevoflurane,particularly sevoflurane postconditioning, remains poorly understood. Therefore, this study was undertaken to probe into the effect of sevoflurane postconditioning on myocardial ischemia-reperfusion injury of children undergoing repair of interventricular septal defect through detecting the levels of CK-MB, cTnl, MDA and activity of SOD in human blood.
METHODS:
Thirty-two (18 male,14 female) children scheduled for elective repair of interventricular septal defect surgery with cardiopulmonary bypass were randomly divided into two groups of 16 children:sevoflurane postconditioning group and control group.In sevoflurane postconditioning group, low tidal volume ventilation was started at 3 min before declamping aorta and at the same time 2.0vol% sevoflurane was inhaled,which lasted to 10 min after declamping aorta. But during this period sevoflurane was not inhaled in control group. The central venous blood samples were collected for the measurements of creatine kinase(CK-MB), cTnI, superoxide dismutase(SOD) and malondialdehyde(MDA) before anesthesia (T1), immediately before clamping aorta(T2), immediately before declamping aorta(T3),5min after declamping aorta (T4), 10min after declamping aorta (T5) and 30min after declamping aorta(T6). HR, MAP and CVP were recorded at T1-T6 also.
RESULTS:
Hemodynamic parameters were kept stable throughout in both groups.
At each period of time after reperfussion, compared with T1, the contents of CK-MB in both groups increased significantly (p<0.05 or 0.01). But compared with control group,the content of CK-MB was significantly lower in SPC group(p<0.05). At each period of time after reperfussion,compared with Tl,the content of cTnl in both groups increased significantly (p<0.01). But compared with control group, the content of cTnl was significantly lower in SPC group(p<0.05).
The MDA in SPC group increased significantly (p<0.05 or 0.01)at T2-T6,compared with that at T1, but at T4-T6, the content of MDA in SPC group was significantly lower than that in control group(p<0.01). At T4-T6, the activity of SOD decreased(p<0.05 or 0.01) in both groups, and SOD in SPC group was higher than that in control group(p<0.01). It is suggested that sevoflurane postconditioning can inhibit increasing of MDA levels to attenuate myocardial ischemia/reperfusion injuries mediated by reactive oxygen series (ROS) during open-heart surgery.
CONCLUSION:
Sevoflurane postconditioning can attenuate myocardial ischeamia-reperfusion injury in children undergoing repair of interventricular septal defect surgery, and.the mechanisms are possiblely related to the antioxidant function of sevoflurane postconditioning.
引文
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[2]Zhao ZQ, Corvera JS, HalkosME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion:comparison with ischemic preconditioning[J]. Am J Physiol Heart Circ Physiol,2003,285 (2):H579-588.
[3]Opie LH. Cardiologists are living through exciting times. The example of postconditioning to protect the human heart during revascularization. Ann Cardiol Angeiol(Paris).2006; 55:64-65.
[4]Venkatapuram S,Wang C, Krolikowski JG, et al. Inhibition of apop totic protein p53 lowers the threshold of isoflurane-induced cardioprotection during early reperfusion in rabbits[J]. Anesth Analg,2006,103 (6):1400-1405.
[5]Obal D,Dettwiler S, Favoccia C, et al. The influence of mitochondrial KATP channels in the cardioprotection of preconditioning and postconditioning by sevoflurane in the rat in vivo [J]. Anesth Analg,2005,101 (5):1252-1260.
[6]Riess ML, Stowe OF, Warltier DC. Cardiac pharmacological preconditioning with volatile anesthetics:from bench to bedside? AmJ Physiol Heart Circ Physiol.2004; 286:H1603-H1607.
[7]Tsutsumi YM, Yokoyama T, Horikawa Y, et al. Reactive oxygen species trigger ischemic and pharmacological postconditioning:in vivo and in vitro characterization[J]. Life Sci,2007,81(15):1223-1227.
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