Stein J H, Osgood R W, Barnes J L, Reineck H J, Pinckard R N, McManus L M
Miner Electrolyte Metab. 1985;11(4):256-61.
One hour occlusion of total renal blood flow results in oliguric acute renal failure as defined by an abrupt and severe diminution in glomerular filtration rate. In rats, after 1-2 h of such ischemia, the acute renal failure which follows is characterized by decreased renal blood flow and by intratubular obstruction with necrotic cellular debris. The present study has examined the possible role of the complement system in the development of this model of acute renal failure. Immunoreactive C3 was extensively localized within necrotic tubular epithelial cells and the walls of small muscular arteries in reperfused kidneys after 1 h of total renal ischemia. Depletion of complement by the administration of cobra venom factor 18 h prior to the induction of ischemia abrogated C3 localization and significantly attenuated the subsequent fall in renal blood flow following reperfusion but did not alter the oliguria or marked fall in glomerular filtration.
完全阻断肾血流1小时会导致少尿型急性肾衰竭，其定义为肾小球滤过率突然且严重降低。在大鼠中，经过1 - 2小时的此类缺血后，随之而来的急性肾衰竭的特征是肾血流量减少以及肾小管内有坏死细胞碎片阻塞。本研究探讨了补体系统在这种急性肾衰竭模型发展过程中可能发挥的作用。在完全肾缺血1小时后再灌注的肾脏中，免疫反应性C3广泛定位在坏死的肾小管上皮细胞和小肌性动脉壁内。在缺血诱导前18小时给予眼镜蛇毒因子以消耗补体，可消除C3的定位，并显著减轻再灌注后随后的肾血流量下降，但并未改变少尿或肾小球滤过的显著下降。
