摘要
目的:本研究旨在探讨心肌再灌注损伤(RI)的机制并评价费乐地平(Felodipine,Fel)对RI的保护作用及其机制。方法:用家兔心肌缺血再灌注模型,分别设对照组、单纯缺血再灌注组及再灌注+Fel治疗组,设再灌注0.5、1.5和6.0小时3个时相点,测定心肌Ca2+、丙二醛(MDA)含量、中性粒细胞(PMN)浸润数、Na+K+ATP酶及Ca2+Mg2+ATP酶活性,并观察心肌超微结构改变及测定心肌梗塞范围。结果:心肌再灌注后Ca2+、MDA含量及PMN浸润数明显增高,Na+K+ATP酶和Ca2+Mg2+ATP酶活性明显降低,其改变以Ca2+升高发生最快;Fel可使上述指标改变的程度明显减轻(P<0.05~0.01),并可缩小心肌梗塞范围,改善其超微结构的变化。结论:心肌RI是多种因素于不同时间所致的一种复合性损伤,Fel对心肌RI有保护作用,其保护机制可能与其对心肌能量依赖性酶活性的改善有关。
Objective:To study the mechanism of myocardial ischemic reperfusion injury (RI) and assess the protective effects of felodipine (Fel) for RI.Methods:The rabbit model of myocardial ischemic reperfusion was used and the rabbits were divided into three groups:simple ischemic reperfusion group (group R),ischemic reperfusion treated with Fel (group R+F) and the control group.At 0.5,1.5,6 0hr after ischemic reperfusion,the contents of myocardial calcium(Ca 2+ ) and malondialdehyde(MDA),infiltration of polymor phonuclear leukocytes(PMNs),activity of Na +K + ATP ase,and Ca 2+ Mg 2+ ATPase were determined.The myocardial ultrastructures and the size of the infarct were evaluated.Results:After myocardial reperfusion,the contents of myocardial Ca 2+ ,MDA and the density of PMNs infiltration were markedly increased and the activity of Na +K +ATPase and Ca 2+ Mg 2+ ATPase were markedly decreased.In group R+F,these changes were significantly mitigated as compared with group R ( P <0.050.01) and the myocardial ultrastructrue was improved and the size of myocardial infarction was reduced .Conclusions:Myocardial RI was a complex injury caused by multiple factors at different times. Fel has a protective effect on the myocardium with RI and the protective mechanism of Fel might be related to the fact that it improves the activity of myocardial Na +K +ATPase and Ca 2+ Mg 2+ ATPase.
出处
《中国危重病急救医学》
CAS
CSCD
1997年第2期67-69,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金
关键词
缺血缺血
再灌注损伤
费乐地平
钙
中性粒细胞
reperfusion injury
felodipine
calcium overload
neutrophilic granulocyte