费乐地平对兔心肌缺血—再灌注损伤的保护作用

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。

Protective effects of felodipine on myocardial ischemia and reperfusion injury in rabbits

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.