异丙肾上腺素ISP致心肌微血管阻塞的机理探讨  

A Pathogenesis of Isoproterenol-induced Occlusion of cardiac Microvasculature in Rats

作　　者：汪学军[1] 欧阳静萍[1] 涂淑珍[1] 刘金保[1] 董传仁[1] 凌宏[1] 

机构地区：[1]湖北医学院病理生理学教研室

出　　处：《微循环学杂志》1992年第1期8-11,共4页Chinese Journal of Microcirculation

摘　　要：本实验通过对血浆凝固性的动态变化和自由基系统有关指标的变化的监测以及心肌组织病理学观察发现,大鼠皮下注射大剂量异丙肾上腺素(ISP)(85mg/kg)后早期(4h以前)即有明显的血浆高凝状态、内源性凝血系统激活和心肌微血管内血栓形成,且心肌缺血损伤程度与血浆凝固性紊乱程度之间呈正直线相关;心、肝、肾和脑以及血清MDA含量显著增加(P<0.01),心肌的SOD和GSH—Px活性均显著增高。提示ISP引起的膜脂质过氧化、血浆高凝状态以及由此而引发的血管内皮受损和微血栓形成是ISP致心肌微血管阻塞的重要机理。This article shows that a severe hypercoagulation of plasma, activation of intrinsic coagulation system and thrombosis in myocardial microvasculature occured during the early period (before 4 bouts) after the rat had been given the hypodermic of isoproterenol (85mg/Kg wet.), and that the severity of the ischemia was closely related to that of dys- function of plasma coagulation. It was also found that the lipid peroxidation products, malonyldialdehyde(MDA) in heart, liver, kidney, brain and serum increased significantly (P<0.01, 0.05), the activity of myocardial superoxide dis- mutase(SOD) and giutathione peroxidase (GSH-Px) increased (P<0.05). The results suggest that the activation of intrin- sic coagulation system and thrombosis in cardiac microvasculature, initiated by free radicals from auto-oxidation of isopro- terenol. be involved in the pathogenesis of occlusion of cardiac microvasculature due to isoproterenol overdosage.

关 键 词：异丙肾上腺素 微血管阻塞 ISP 机理探讨 微血管内血栓形成 血清MDA含量 凝血系统激活 膜脂质过氧化 高凝状态 病理学观察 自由基系统 正直线相关 微血栓形成 心肌组织 动态变化 皮下注射 损伤程度 心肌缺血 内皮受损 血浆 

分 类 号：R285.5[医药卫生—中药学] R542.22[医药卫生—中医学]