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内皮素和一氧化氮在腺嘌呤所致急性肾衰模型中的作用 被引量:2

Roles of endothelin and nitrogen monoxide in the adenine-induced acute renal failure models
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摘要 目的 :探讨内皮素 (ET)及一氧化氮 (NO)在急性肾衰 (ARF)中的作用。方法 :4 0只雄性Wistar大鼠分为5组 ,后 4组用腺嘌呤加入饲料中喂养 ,制作肾内梗阻性急性肾衰模型 ,用NADPH 黄递酶染色法测定肾组织NOS活性 ,采用免疫组化ABC法测定肾组织ET 1的表达 ,采用CMM3型病理图像分析系统 ,进行染色后切片的平均光密度测定。结果 :ET 1在正常鼠肾组织表达广泛而弱 ,而ARF时髓质部位ET 1表达明显增强 (P <0 .0 5 ) ,皮质无明显变化。鼠肾各层NOS活性明显降低 (P <0 .0 5 )。ARF鼠予以L 精氨酸治疗后 ,血尿素氮、肌酐和尿素等指标有改善 (P<0 .0 1) ,但ET 1,NOS在肾组织表达无改善。当停止给ARF鼠喂养腺嘌呤后 ,尿比重、尿钠、血尿素氮、肌酐和尿素等指标逐步恢复正常 ,肾组织ET 1和NOS的表达也恢复正常。结论 :ET 1及NO可能参与了肾内梗阻型急性肾衰的发生、发展和转归 ;L 精氨酸可能对ARF鼠肾功能有一定保护作用。 Objective To determine the roles of endothelin(ET) and nitrogen monoxide(NO) in the adenine-induced acute renal failure(ARF) models. Methods ARF models were established by feeding adenine in rats. The activity of NO synthase (NOS) in kidneys of rats was tested by NADPH- diaphorase . Expression of endothelin-1 (ET-1)in kidneys of rats was studied by immunoreactivity method. The area densities for ET-1 and NOS expressions in kidneys were determined by CMM3 pathology image analysis system to calculate the mean light density.Results Expressions of ET-1 in normal rat kidneys were wide and weak, but they were greatly enhanced in medulla renis of the ARF models while remained unchanged in the cortex.The activities of NOS were stronger in the cortex and the inner medulla than in the outer medulla. The renal functions of the ARF models were improved after they were treated with L-argine, but the expressions of ET-1 and NOS were not improved.After the withdrawal of adenine, the ARF model rats recovered gradually in their renal functions, and the same was true for the expressions of ET-l and NOS.Conclusion ET-1 and NO both play important roles in the occurrence, development and recovery of ARF. It is supposed that L-Arg can partly protect the renal functions of ARF rats.
出处 《中南大学学报(医学版)》 CAS CSCD 北大核心 2004年第3期292-296,共5页 Journal of Central South University :Medical Science
关键词 内皮素 一氧化氮 ET NO 腺嘌呤 急性肾衰模型 ARF acute renal failure adenine endothelin nitric oxide synthase
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