依地酸3,6-二甲基氨基二苯并吡啶鎓对整体缺血再灌注离体大鼠心脏的保护作用。

Protective effects of 3,6-dimethylamino-dibenzopyriodonium edetate on global ischemia reperfused isolated rat hearts.

作者信息

Ji G J, Zhang J Z, Liu D Q, Zhao D H, Sheng B H

机构信息

Department of Pharmacology, Medical College of General Logistics Department, PLA, Beijing, China.

出版信息

Zhongguo Yao Li Xue Bao. 1993 May;14(3):206-10.

PMID:8237392

Abstract

The effects of 3,6-dimethylamino-dibenzopyriodonium edetate (IHC-72) on global ischemia reperfused rat hearts were investigated. In the isolated working rat heart, 40-min global ischemia followed by 30-min reperfusion resulted in increases of ventricular tachycardia (VT) and ventricular fibrillation (VF), increases of creatine kinase (CK) release and malondialdehyde (MDA) contents, but decreased superoxide dismutase (SOD) activity. Following ischemia and reperfusion, the accumulation of myocardial calcium increased. IHC-72 50 mumol.L-1 given 10 min before ischemia and during reperfusion decreased the cardiac CK release, VT, and VF, reduced the MDA contents, prevented the reduction of SOD activity and attenuated the accumulation of myocardial calcium and sodium vs control. These results indicated that IHC-72 protected myocardial reperfused injury.

摘要

研究了依地酸3,6-二甲基氨基二苯并吡啶鎓（IHC-72）对全脑缺血再灌注大鼠心脏的影响。在离体工作大鼠心脏中，40分钟全脑缺血后再灌注30分钟导致室性心动过速（VT）和室颤（VF）增加、肌酸激酶（CK）释放增加和丙二醛（MDA）含量增加，但超氧化物歧化酶（SOD）活性降低。缺血再灌注后，心肌钙的积累增加。在缺血前10分钟和再灌注期间给予50μmol.L-1的IHC-72，与对照组相比，可降低心脏CK释放、VT和VF，降低MDA含量，防止SOD活性降低，并减轻心肌钙和钠的积累。这些结果表明，IHC-72可保护心肌再灌注损伤。