摘要
依据运动性肾缺血再灌的理论,探讨了运动性蛋白尿的发生机制。利用 ESR 技术报导了肾脏出现的新的自由基信号,同时观察了运动前后肾线粒体膜和肾组织超微结构的改变,认为运动后引起的尿TP、ALb、β(?)MG 排泄率增加和上述反应密切相关。提示:OFR 引发的肾脏脂质过氧化反应可能是运动性蛋白尿形成的重要因素之一。
In this research 24 trained male SD rats were randomly divided into three groups:1.exercise(with USP injections) group,2.recovery(30 minutes after exercise)group and 3.control group.The exercise load was 35 m/min running on a treadmill.Renal tissue samples were monitored with electron spin resonance(ESR)at 100K.Changes in the supermicrostructure of the kidneys were observed.Meanwhile,LPO,SOD,TP,Alb,β_2—MG werealso measured.The results indicated that the decrease in renal blood flow during exercise and reperfusion afterexercise recovery may be the important factor leading to the post-exercise proteinuria.The process conforms tothe general rule of ischemia reperfusion injury by the oxygen free radicals induced.
出处
《体育科学》
CSSCI
北大核心
1993年第1期53-55,58+95,共5页
China Sport Science
关键词
蛋白尿
缺血再灌
氧自由基
proteinuria,ischemia reperfusion,oxygen free radicals.