Garcia-Estan J, Roman R J, Lianos E A, Garancis J
Department of Physiology, Medical College of Wisconsin, Milwaukee.
J Lab Clin Med. 1989 Oct;114(4):389-93.
The role of complement in mediating the changes in renal hemodynamics and glomerular eicosanoid synthesis after the administration of heterologous antibody against rat glomerular basement membrane (AGBM) was studied in Munich-Wistar rats. AGBM serum decreased glomerular filtration rate (GFR) and increased glomerular thomboxane B2 (TxB2) production without associated changes in glomerular prostaglandin E2 (PGE2) or PGF2 alpha production. Pretreatment of rats with cobra venom factor to deplete complement blocked the fall in GFR produced by AGBM without altering the increment in glomerular TxB2 production. In these animals, glomerular PGE2 synthesis was elevated. The results indicate that the salutary effects of complement depletion in nephrotoxic serum nephritis are not mediated by changes in the glomerular production of the vasoconstrictor TxA2. An enhanced production of PGE2 may participate in preventing the fall in GFR after AGBM administration in the complement-depleted rats.
在慕尼黑-威斯塔大鼠中研究了补体在注射抗大鼠肾小球基底膜（AGBM）异源抗体后介导肾脏血流动力学变化和肾小球类花生酸合成中的作用。AGBM血清降低了肾小球滤过率（GFR）并增加了肾小球血栓素B2（TxB2）的产生，而肾小球前列腺素E2（PGE2）或前列腺素F2α的产生没有相关变化。用眼镜蛇毒因子预处理大鼠以消耗补体，可阻断AGBM引起的GFR下降，而不改变肾小球TxB2产生的增加。在这些动物中，肾小球PGE2合成升高。结果表明，补体消耗在肾毒性血清肾炎中的有益作用不是由血管收缩剂TxA2的肾小球产生变化介导的。PGE2产生的增加可能参与防止补体消耗的大鼠注射AGBM后GFR的下降。
