Limb ischemic postconditioning protects myocardium from ischemia-reperfusion injury
Limb ischemic postconditioning protects myocardium from ischemia-reperfusion injury
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DOI：
10.1080/14017430600925292
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发表时间：
2006-10-01
影响因子：
2.2
通讯作者：
Luo, Man
中科院分区：
文献类型：
--
作者：
Li, Chun-Mei;Zhang, Xing-Hua;Luo, Man
目标。验证肢体缺血后处理对心肌再灌注损伤的保护作用，并探讨其机制。设计。将40只大白兔随机分为4组：对照组、缺血预适应组、缺血后处理组和远程后处理组。实验结束时测定心肌梗死面积和组织髓过氧化物酶活性。分别于基础、缺血结束和再灌流3h后测定血浆肌酸激酶和丙二醛活性。结果。与对照组相比，缺血预适应组、缺血后处理组和远程后处理组的心肌梗死面积显著减少(p<；0.01)。结果由血浆肌酸激酶活性证实。缺血预适应组、缺血后处理组和远隔后处理组再灌注3h血浆丙二醛水平显著低于对照组(p<；0.01)。缺血预适应组、缺血后处理组和远隔后处理组的中性粒细胞积聚(髓过氧化物酶活性)明显低于对照组(p<；0.01)。结论。远程后处理可减少兔心肌梗死。其机制可能与减轻氧自由基损伤和提高抗氧化作用有关。
Objective. To test the hypothesis that limb ischemic postconditioning protects the myocardium from reperfusion injury, and examine the mechanism involved. Design. Forty rabbits were randomly divided into four groups: Control, Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning. Myocardial infarct size and tissue myeloperoxidase activity were determined at the end of the experiment. Plasma creatine kinase and malondialdehyde activity were measured at baseline, the end of ischemia, and after 3 h of reperfusion respectively. Results. Myocardial infarct size was significantly reduced in Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning as compared to Control (p < 0.01). Results were confirmed by plasma creatine kinase activity. Plasma malondialdehyde was significantly less at 3 h of reperfusion in Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning than that in Control (p < 0.01). Neutrophil accumulation (myeloperoxidase activity) in the area at risk was less in Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning than that in Control (p < 0.01). Conclusion. Remote postconditioning reduces myocardial infarction in rabbits. The mechanism involved might be reduced oxygen radical-induced injury and improved antioxidant action.