摘要
目的观察缺血预处理(IPC)对体外循环中缺血再灌注心肌组织磷酯酶A2(PLA2)和ATPase活性的影响,评价其对心肌的保护作用,并初步探讨其作用机制。方法90只家猫制备体外循环模型,将随机均分3组:单纯体外循环(CPB)组、主动脉阻断组和IPC组。分别测定体外循环时心肌组织PLA2及Na+K+ATPase、Ca2+Mg2+ATPase、Ca2+ATPase的活性,比较各组心肌PLA2及各ATPase活性的变化。结果IPC组可明显减轻CPB时缺血再灌注导致的PLA2活性升高和ATPase活性下降。结论IPC可能通过减轻缺血再灌注期间的Ca2+超载及抑制细胞膜磷脂水解而发挥其心肌保护作用。
Objective To elucidate the influences of ischemic preconditioning(IPC) on activity of phospholipase A2 and ATPase of ischemia/reperfusion myocardial cell during cardiopulmonary bypass (CPB). Methods Ninety felines were randomized into there groups: group A(n=30), in which CPB was conducted without aortic cross-clamping(ACC) ; group B(n=30), with 60 min ACC followed by 90 min reperfusion, and cardioplegia used during period of ACC; group C(n= 30), with protocol similar to that of group B except for three-round (5 min block and 10 min open blood flow) 15 min IPC applied before ACC. Activities of PLA2 and Na^+-K^+-ATPase, Ca^2+-Mg^2+-ATPase and Ca^2+-ATPase of myocardial cells were simultaneously measured during ACC and reperfusion periods. Results IPC significafitly alleviated the upregulated activity of PLA2 and the inhibited activities of Na^+-K^+-ATPase, Ca^2+-Mg^2+-AT Pase and Ca^2+-ATPase of myocardium during periods of ischemia and reperfusion. Conclusion IPC can protect myocardial cells from ischemia and reperfusion injury which may due to alleviation of Ca^2+ overload and hydrolysis of membrane phospholipid by regulating the activities of PLA2 and the ATPases of myocardium.
出处
《福建医科大学学报》
2006年第2期118-120,共3页
Journal of Fujian Medical University
基金
福建省自然科学基金资助项目(C0110026)
关键词
心肺转流术
心肌再灌注损伤
磷酯酶类
腺苷三磷酸酶
缺血预处理
猫
cardiopulmonary bypass
myocardial reperfusion injury
phospholipases
ATPase
ischemic preconditioning
cats