目的 :观察内皮素受体拮抗剂PD14 50 65联合内皮源血管松驰因子NO生理性前体L -arginine对大鼠缺血性急性肾衰竭是否有防治作用。方法 :采用阻断大鼠双侧肾脏血流 4 5min再灌注 2 4h之急性肾缺血再灌注动物模型 ,观察内皮素受体拮抗剂PD14 50 65或内皮源血管松驰因子NO生理性前体L -arginine或两者联合应用 ,对再灌注2 4h后大鼠肾组织病理变化和肾功能的影响。结果 :PD14 50 65或L -arginine单独作用均可明显减轻肾缺血再灌注后的肾组织病理损害 ,提高肾小球滤过率 ,改善肾功能。其中 ,两者联合应用的效果比单独使用的效果更好。结论 :缺血性急性肾衰竭时 ,内皮素升高及其受体上调是缺血性急性肾衰竭发生发展的重要因素 ,外源性给予内皮素受体拮抗剂可阻断内皮素的生物作用 ,并且联合内皮源血管松弛因子的应用效果更佳。这是防治缺血性急性肾衰竭的又一新途径。 Objective: To observe whether endothelin receptor antagonist PD14 50 65 combined with endothelium-derived vascular relaxation factor NO physiological precursor L-arginine can prevent and cure acute ischemic renal failure in rats. Methods: Animal models of acute renal ischemia-reperfusion injury were established by blocking the bilateral renal blood flow for 45 min and reperfusion for 24 h. The effects of endothelin receptor antagonist PD14 50 65 or endothelium-derived vascular relaxation factor NO precursor L-arginine or a combination of the two on rat renal tissue pathological changes and renal function after 24 hours of reperfusion. Results: PD14 50 65 alone or L-arginine alone could significantly reduce the pathological changes of renal tissue after renal ischemia / reperfusion, improve glomerular filtration rate and improve renal function. Among them, the combined effect of the two is better than the single effect. Conclusions: Elevated endothelin and its receptor upregulation is an important factor in the development of ischemic acute renal failure in ischemic acute renal failure. Exogenous administration of endothelin receptor antagonist can block the biological effect of endothelin , And combined with endothelium-derived vascular relaxation factor application effect is better. This is another new way to prevent ischemic acute renal failure.