GIK对大鼠离体心脏缺血再灌注损伤保护作用的研究  

Protective effects of glucoseinsulinpotassium on myocardial injury after ischemia/reperfusion in isolated rat heart

作　　者：曹新来[1,2] 刘桥义[1,2] 

机构地区：[1]第三军医大学附属新桥医院麻醉科 [2]北京304医院麻醉科

出　　处：《第三军医大学学报》1997年第3期237-239,共3页Journal of Third Military Medical University

摘　　要：目的：研究葡萄糖－胰岛素－氯化钾（ＧＩＫ）对大鼠离体心脏缺血再灌注损伤的影响，为临床体外循环心脏瓣膜替换术应用ＧＩＫ提供依据。方法：４２只大鼠随机分为对照组、缺血再灌注组与ＧＩＫ防护组，处死动物后迅速取出心，制成离体心脏作功模型，测定心功能指标与心肌电镜检查。结果：缺血再灌注明显降低心率、左室收缩压、室内压变化速率、冠脉流量、增加左室终末舒张压及乳酸脱氢酶释放量、明显损害心肌超微结构。而ＧＩＫ能使以上指标在缺血再灌注后仍保持在对照组水平。结论：ＧＩＫ可预防缺血再灌注对心肌的损伤作用，并改善离体作功心脏的功能。Objective: To explore the protective effects of glucoseinsulinpotassium (GIK) on myocardial damage after ischemia/ reperfusion. Methods: After 42 rats were randomized into the control, ischemia/reperfusion and GIKtreated groups, the animals were killed to establish the model of isolated working heart with Langendorff device. Then the parameters of heart function and activity of LDH were determined with biochemical assay and the changes of myocardial ultrastructure observed with electron microscopy. Results: Ischemia/reperfusion induced the obvious decrease in HR, LVSP, (dp/dt max, CF and CO, increased LVEDP and activity of LDH in coronary flow and damaged myocardial ultrastructure. But no significant changes were found in GIKtreatecd group and the control group. Conclusion: GIK can prevent myocardium from injury after ischemia/reperfusion and improve the function of the isolated working heart.

关 键 词：再灌流损伤 葡萄糖 胰岛素 心肌缺血 GIK 

分 类 号：R542.205[医药卫生—心血管疾病]