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观察心肌局部肾素－血管紧张素系统（ＲＡＳ）在心肌缺血再灌注损伤时的激活情况及特异性非肽类血管紧张素Ⅱ１型受体（ＡＴ１）阻断剂Ｌｏｓａｒｔａｎ的保护效应。方法离体大鼠心脏灌流模型，心功能测定，放射免疫测定。结果心肌缺血４０ｍｉｎ后，心肌内ＡｎｇⅡ即明显增高（Ｐ＜０．０１），ＡｎｇⅠ增高尚不明显；再灌１０ｍｉｎ后，ＡｎｇⅠ、ＡｎｇⅡ均明显升高（Ｐ＜０．０１），Ｌｏｓａｒｔａｎ５μｍｏｌ／Ｌ不明显影响这种增高，但却能使缺血再灌注损伤后的心功能得到明显改善，减少心肌肌酸激酶（ＣＫ）的释放。结论一定时间的缺血和再灌注均能使心肌组织中ＲＡＳ有所激活，ＡｎｇⅡ增高可加重缺血心肌的损伤，Ｌｏｓａｒｔａｎ通过特异阻断ＡＴ１受体有减轻这种损伤的作用
To observe the activation of myocardial renin-angiotensin system (RAS) during myocardial ischemia-reperfusion injury and the protective effect of Losartan, a specific non-peptide angiotensin Ⅱ type 1 receptor (AT1) antagonist. Methods Isolated rat heart perfusion model, cardiac function, radioimmunoassay. Results After myocardial ischemia for 40min, AngⅡ was significantly increased in myocardium (P <0.01), but not in Ang Ⅰ. After reperfusion for 10min, AngⅠ and AngⅡ were significantly increased (P <0.01); Losartan 5μmol / L Not significantly affect this increase, but it can make the heart function after ischemia-reperfusion injury was significantly improved, reduce myocardial creatine kinase (CK) release. Conclusions Both ischemia and reperfusion can activate RAS in myocardial tissue for a certain period of time. Increased Ang Ⅱ may aggravate the injury of ischemic myocardium. Losartan can attenuate this damage by specifically blocking AT1 receptor