卡托普利对Langendorff灌注大鼠全心缺血-再灌注损伤的保护作用

目的：探讨卡托普利对Langendorff灌注大鼠全心缺血-再灌注损伤的保护作用及机制。方法：采用Langendorff离体全心灌流装置，模拟缺血-再灌注，观察卡托普利对大鼠全心缺血-再灌注引起的心律失常的作用及体内CPK、LDH、MDA、SOD及AngⅡ含量的变化。结果：卡托普利减少缺血及再灌注期心律失常的发生，加快再灌注期高度房室传导阻滞的恢复。缺血期：CPK及LDH缺血-再灌注(B组)组较对照组(A组)明显增加，卡托普利治疗组(C组)较B组显著降低，再灌注期：CPK及LDH B组较A组明显增加，C组较B组明显降低，心肌组织MDA，Ang II的含量B组明显高于A组，C组明显低于B组，而SOD含量两组比较无显著性差异。结论：卡托普利具有拮抗离体大鼠全心缺血一再灌注损伤的作用，拮抗作用是通过抑制血管紧张素转换酶(ACE)而抑制Ang II的生成，抑制氧自由基的产生而实现的。

Cardioprotective of Captopril on Langendorff Perfused Ischemic Reperfusion Injury in Whole Isolated Rat Hearts

Objective:To investigate the cardioprotective and mechanisms of Captopril on Langendorff per-fused in whole isolated rat hearts.Methods:Langendorff perfused system was used to investigate the effect of Captopril on CPK,LDH,MDA,SOD,and Ang II in whole isolated rat hearts and occurrence of arrhythmi-a.Results:Captopril decreased incidence of arrhythmia in ischemic and reperfusion periods,and improved atrial ventricular block recovery in reperfusion period.During ischemic period,CPK and LDH in group B increased significantly compared with that in group A,but greatly decreased in group C compared with that in group B.During reperfusion period,CPK and LDH increased significantly in group B compared with that in group A,however decreased in group C compared with that in group B.The contents of MDA and Ang II of myocardial tissue in group B were higher than that in group A.The content of MDA of myocardial tissue in group C was much lower than that in group A.The content of MDA of myocardial tissue in group C was much lower than that in group A.SOD had no significant change in two groups.Conclusion:Captopril against is-chemic_reperfusion injury in whole isolated rat hearts,those beneficial effects are mediate primarily by the in-hibition of Angiotensin II formation and inhibited oxygen free radical scavenging potential.