摘要
目的 观察缺血预适应(IPC) 在结合低温高钾时的心肌保护作用并探讨其机制。方法 采用离体大鼠心脏非工作模型。将48 只SD 大鼠随机分为4 组( 每组12 只) 。A 组(control) 为实验对照组;B 组(IPC) ,37 ℃下行单次5 min 停灌注加5 min 再灌注,建立IPC;C 组( 腺苷受体非选择阻断剂苯茶碱加IPC) 建立IPC 前预灌苯茶碱(100 μmol·L-1)5 min ;D组( 腺苷) ,预灌腺苷(10 μmol·L-1)5 min 。4 组心脏全心缺血90 min 再灌注30 min ,记录缺血前及再灌注期的左心功能指标,辅以心肌酶学及超微结构观察。结果 B 组于再灌注期左心功能恢复情况优于其他各组( P< 0 .05) ,C、D 两组优于A 组( P< 0 .05) 。酶学及超微结构检查示B 组损伤最轻。结论 IPC 在结合低温高钾停搏条件下,能明显促进缺血再灌注后心脏功能恢复,腺苷是参与IPC
Objective To investigate the cardioprotection of ischemic preconditioning and its mechanism. Methods 48 isolated rat hearts were divided into four groups of 12 each. In group A(control) hearts were untreated and served as controls during preischemic period.In group B (IPC),hearts were preconditioned with 5?min of global ischemia followed by 5min of reperfusion before the onset of cardioplegic arrest. In group C (8-PTH+IPC),hearts were given 8-PTH(100μm) for 5?min before ischemic preconditioning. In group D (ADO),hearts were perfused with ADO (10?μm) for 5?min before cardioplegic arrest. Four groups of hearts were subjected to 90?min hypothermic ischemic and 30?min reperfusion. Functional measurements were taken during the stable period and repeated at 10,30?min of reperfusion. Enzyme leakage and ultrastructural alterations in the myocardium were examined.Results The results indicated that recovery of left ventricular function was much better in group B than in other groups ( P <0.05) during reperfusion. They were better in group D and C when compared with group A ( P <0.05).Conclusions IPC obviously can promote the recovery of myocardium from ischemic reperfusion injury. The mechanism of preconditioning is partly mediated by adenosine receptors in the rat model.
出处
《铁道医学》
1999年第6期376-378,共3页
Railway Medical Journal
关键词
缺血预适应
心肌保护
再灌注损伤
大鼠
ischemic preconditioning myocardial protection reperfusion injury of myocardium adenosine isolated heart rats
