血管紧张素Ⅱ预处理对大鼠缺血再灌注损伤心脏的保护作用

Effect of cardioprotection with AngⅡ preteatment on myocardial ischemia-reperfusion injury in rat

许多证据表明，心肌缺血再灌注损伤过程中，心脏局部肾素血管紧张素系统(RAS)被激活，局部增多的血管紧张素Ⅱ(AngⅡ)会对心脏产生进一步的损害作用。于是认为，如果在缺血再灌注前给予外源性AngⅡ势必会加重心肌的损害。然而，我们的研究却表明，大鼠离体心脏缺血前随灌流液给予1nmol/L AngⅡ 5min灌流，然后再给5min正常灌流不但对随后40min缺血及20min再灌注的心肌没有加重损伤，反而对心脏有一定的保护作用，且这种效应不被AT1受体阻断剂Losartan阻断。由此推测，缺血前给予少量的外源性AngⅡ有可能通过非AT1途径对心脏发挥保护作用。其机制可能与缺血性预处理的某些过程有关，其意义和机理值得进一步探讨。

There is now evidence that the local intracardiac reni n angiotensin system (RAS) is a ctivated during the period of myocardial ischemi a and reperfusion, and the increased endogenous AngⅡ in cardiac tissues was lik ely to accelerate the myocardial damage. Therefore, there may be a more deleter ious effect of exogenous AngⅡ on myocardial ischemia-reperfusion injury. Howe ver, our study demonstrated that 5 min perfusion of 1nmol/L AngⅡ following 5 mi n normal KH perfusion before ischemia could attenuate myocardial injury subseque ntly after 40 min myocardial ischemia and 20 min reperfusion in rat, and Losarta n couldn’t antagonize such effect, implying that minor exogenous AngⅡ prior to ischemia may have some cardioprotective effect related to ischemic precondition ing. The mechanism needs further study.