API_(0134)对缺血一再灌注心肌氧自由基和钙超负荷的作用

An Experimental Study of the Effect of API_(0134) on the Oxygen Free Radicals and Ca^(2+) Overloading in the Process of Myocardial Ischemia Reperfusion

在犬急性心肌缺血一再灌注模型上，结扎冠状动脉左前降支（LAD）90min后，行再灌注120min。发现缺血区心肌组织超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH－Px）活性降低，丙二醛（MDA）含量增加（均为P＜0．05）；Na+、Ca(2+)含量明显增加，K+含量及K+／Na+比值显著降低（均为P＜0．01）。再灌注前45min静脉给予API(0134)，则见相应的缺血区SOD、GSH－Px活性。K+含量及K+／Na+比值高于对照组（P＜0．05或P＜0．01），而MDA和Na+、Ca(2+)含量明显低于对照组。说明API(0134)能防治再灌注损伤，这与它减轻氧自由基的危害，降低组织钙超负荷有关。

In the acute ischemia reperfusion dog model after ligating of LAD for 90 min reperfusion was established for 120 min. The results showed that the activity of SOD, GSH-Px in ischemic myocardial area was decreased, MDA level increased (P<0. 05), besides, Na+ and Ca2+ level increased markedly, K+ and K+ /Na+ decreased significantly (P<0. 05 ).In the API(0134)-treated group, in which API(0134) was infused 45min before reperfusion, the activity of SOD, GSH-Px and the level of K+and K+/Na+ were higher than those in the control group, the concentration of MDA, Na+, and Ca2+ was lower. These data suggest that API(0134)may have protective effect on myocardial ischemic reperfusion injury. The mechanism may be related to its alleviation of harmful effect induced by oxygen free radical and Ca2+-overloading.