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目的探讨血管紧张素-(1-7)对心肌肥厚大鼠体外心脏缺血再灌注损伤的影响。方法通过腹主动脉结扎制作大鼠心肌肥厚模型,并用Langendorff装置建立心肌肥厚大鼠体外心脏缺血再灌注模型,观察血管紧张素-(1-7)对心肌肥厚大鼠体外缺血再灌注心脏左心室收缩压、冠状动脉流量、肌酸磷酸激酶和乳酸脱氢酶释放、心肌梗死范围的影响。结果与缺血再灌注对照组相比,血管紧张素-(1-7)处理组心脏左心室收缩压、冠状动脉流量显著提高,冠状动脉循环流出液中肌酸磷酸激酶、乳酸脱氢酶含量降低,心肌梗死范围减小。血管紧张素-(1-7)受体拮抗剂A779能够消除血管紧张素-(1-7)的这种心脏保护作用。结论血管紧张素-(1-7)能够减轻心肌肥厚大鼠体外心脏缺血再灌注损伤,其作用通过其特异性受体介导。
Objective To investigate the effect of angiotensin - (1-7) on myocardial ischemia reperfusion injury in isolated hypertrophic rats. Methods Rat model of myocardial hypertrophy was established by ligation of the abdominal aorta. The model of myocardial ischemia / reperfusion in rats with cardiac hypertrophy was established by Langendorff apparatus. The effects of angiotensin- (1-7) on myocardial ischemia-reperfusion in vitro Left ventricular systolic pressure, coronary flow, creatine phosphokinase and lactate dehydrogenase release, myocardial infarct size. Results Compared with ischemia / reperfusion control group, left ventricular systolic pressure and coronary flow were significantly increased in angiotensin - (1-7) - treated group. Creatine phosphokinase and lactate dehydrogenase Reduce, reduce the scope of myocardial infarction. Angiotensin- (1-7) receptor antagonist A779 abolished this cardioprotective effect of angiotensin- (1-7). CONCLUSION Angiotensin- (1-7) can attenuate cardiac ischemia-reperfusion injury in vitro in hypertrophic rats and its effect is mediated by its specific receptor.