心肌缺血预处理延迟保护作用的实验研究

本实验旨在探讨心肌缺血预处理延迟保护的作用机制。采用大鼠心脏缺血预处理模型，检测缺血预处理后即刻、１２、２４、４８和７２ｈ各时相点再行心肌缺血１ｈ复灌１２ｈ时心肌细胞间粘附分子（ＩＣＡＭ－１）的表达及心肌梗塞范围、超氧化物歧化酶（ＳＯＤ）含量及白细胞（ＰＭＮｓ）浸润数的变化。结果显示，与单纯缺血再灌注组比较，预处理后２４～７２ｈＩＣＡＭ－１表达明显减少，ＳＯＤ含量增高，ＰＭＮ浸润数减少，心肌梗塞范围缩小（Ｐ＜０．０５），以４８ｈ最显著。本实验表明，预处理后２４～７２ｈ心肌对再次长时间缺血／再灌注的损伤有保护作用，其产生可能与ＩＣＡＭ－１表达降低所介导的ＰＭＮｓ浸润减少及ＳＯＤ含量增加有关

Experimental Study on the Delayed Protection of Myocardial Ischemic Preconditioning

This experiment is attempt to explore the mechanism of delayed protection (DP) of ischemic preconditioning(IPC).In the IPC model,myocardial expression of intercellar adhesion molecules(ICAM-1),the content of superoxides dismutase(SOD),polymorphonuclear leukocytes(PMNs) and the infarct size were detemined at the end of 1h myocardial ischemia followed by 12h reperfusion after\ IPC\ 0,12h,24h,48h,72h.The results showed that in IPC group,ICAM-1 expression,PMN infiltration and infarct size were significantly decreased and SOD contents were increased as compared with that in I/R(Ischemia/Reperfusion) group P<0.05.The most significant difference occur at 48h after IPC. but no difference was observed at 12h after IPC.So we concluded that DP was induced by IPC occur at 24～72 hours after IPC ,and that was associated with the decreased ICAM-1 expression and PMNs infiltration,and increased SOD contents . \ \