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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。
Many evidences indicate that during the process of myocardial ischemia-reperfusion injury, the local renin-angiotensin system (RAS) is activated and locally increased angiotensin II (AngⅡ) may cause further damage to the heart. So that if administered before exogenous Ang Ⅱ ischemia is bound to aggravate myocardial damage. However, our study showed that perfusion of 1 nmol / L Ang II for 5 minutes before perfusion in rat hearts and subsequent normal perfusion for 5 minutes did not cause any aggravating damage to the myocardium following 40 minutes of ischemia and 20 minutes of reperfusion. Instead, The heart has a protective effect, and this effect is not blocked by the AT1 receptor blocker Losartan. It is speculated that given a small amount of exogenous Ang Ⅱ before ischemia may play a protective role in the heart through non-AT1 pathway. The mechanism may be related to some processes of ischemic preconditioning, its significance and mechanism worth further study.