缺血预处理和外源性左族精氨酸减小家兔心肌梗塞范围  

ISCHEMIC PRECONDITIONING AND EXOGENOUS L-ARGININE REDUCE INFARCT SIZE IN RABBIT HEART

作　　者：丁延峰[1] 李玉龙[1] 何瑞荣[1] 

机构地区：[1]河北医科大学基础医学研究所生理室

出　　处：《生理学报》1996年第6期564-570,共7页Acta Physiologica Sinica

摘　　要：在麻醉家兔心肌缺血－再灌注（ＩＲ）模型上，观察ＮＯ前体左旋精氨酸（Ｌ－ａｒｇ）、缺血预处理（ＩＰ）对血流动力学和心肌梗塞范围的影响，旨在阐明外源性Ｌ－ａｒｇ对家兔ＩＲ心肌有无保护作用，并探讨Ｌ－ａｒｇ－ＮＯ通路是否参与ＩＰ的心肌保护效应。所得结果如下：（１）在单纯缺血（３ｍｉｎ）－再灌注（１８０ｍｉｎ）过程中，血压、心率和心肌耗氧量呈进行性降低，心肌梗塞范围占左心室的３３．９±２．４％。（２）静注Ｌ－ａｒｇ（３００ｍｇ／ｋｇ）后再进行ＩＲ时，心肌梗塞范围为２０．１±２．２％，较单纯ＩＲ时明显减小（Ｐ＜０．０１），预先静注ＮＯ合成酶抑制剂硝基左旋精氨酸（Ｌ－ＮＮＡ），得以取消上述Ｌ－ａｒｇ对心肌的保护作用，说明外源性Ｌ－ａｒｇ对ＩＲ心肌的保护作用是通过Ｌ－ａｒｇ－ＮＯ通路实现的。（３）ＩＰ时心肌梗塞范围为２１．９±２．１％，较单纯ＩＲ组的显著缩小（Ｐ＜０．０１），表明ＩＰ对ＩＲ心肌有明显保护效应。Ｌ－ＮＮＡ不能阻止ＩＰ的心肌保护作用，提示心脏内的Ｌ－ａｒｇ－ＮＯ通路不参与ＩＰ的效应。（４）外源性Ｌ－ａｒｇ得以加强ＩＰ的心肌保护效应。以上结果表明：外源性Ｌ－ａｒｇ对ＩＲ心肌的保护是通过Ｌ－ａｒｇ－ＮＯ通路实现的?The effects of NO donor-L-arginine (L-arg) and ischemic preconditioning (IP)on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia- repefusion to define whether exogenous L-argcould exert a beneficial effect in this pathological model, and whether the L-arg-NOpathway was involved in the cardioprotection provided by IP. The results obtained wereas follows: (1) During the course of ischemia (30 min) -reperfusion (180 min), bloodpressure, heart rate and myocardial oxygen consumption decreased progressively, andthe myocardial infarct size occupied 33. 9 f 2. 4 % of the whole left ventricle. (2) Themyocardial infarct size could be reduced to 20. 1 ± 2. 2 % (P<0. 01 ) by pretreatmentwith L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished byNO synthesis inhibitor - Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21. 9±2. 1 % (P<0. 01 ), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it wasimplied that the L-arg-NO pathway was not involved in the cardioprotective mechanismof iP. (4 ) Exogenous L-arg might markedly augment cardioprotection provided by IP.The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfused myocardium was mediated by L-arg-NO pathway, which, however, wasnot involved in the cardioprotection provided by IP.

关 键 词：心肌梗塞 缺血预处理 左旋精氨酸 

分 类 号：R542.220.2[医药卫生—心血管疾病]