摘要
本文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技术报导了运动后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_2-MG排泄率增加和上述反应密切相关。提示:运动后OFR产生与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 paper, the mechanism of postexercise proteinuria was studied bas-ed on the theory of ischemic reperfusion.The parameters observed at rest(Grp 1), 30 minutes after exercise ( Grp 2 ) and allopurinol injected after ex-ercise ( Grp 3 ) included renal supermicrostructure, lipid fluidity ( LFD), lipidperoxide ( LPO ) and superoxide dismutase ( SOD ) of renal mitochondrial mem-brane: the exertion rate of urinary total protein(TP), albumin ( ALB ) and β 2-macroglobulin ( β_2-MG).The results were as follows:1. A sharp major free ra-dical signal in Electron Spin Resonance(ESR)was found in Grp 2; 2. Comparedwith Grp 1, the SOD and LFD decreased ( p<0.01 ) following apparent increaseof LPO level in Grp 2 (p<0.01); 3. Compared with Grp l and 3, urinaryexertion of TP, ALB and β 2-MG increased in Grp 2 (p<0.01); 4. The renalmorphological changes were slight. It was concluded that the production ofrenal free radical might be caused by renal ischemic reperfusion.The decreaseof the renal blood flow during exercise and the reperfusion after exercise mightbe the important factors of the postexercise proteinuria.
出处
《中国运动医学杂志》
CAS
CSCD
北大核心
1993年第4期215-218,共4页
Chinese Journal of Sports Medicine
关键词
蛋白尿
缺血再灌注
自由基
proteinuria
ischemia reperfusion
free radical
