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大鼠甘油诱导的 established 急性肾衰竭中的肾小球血流动力学

Glomerular hemodynamics in established glycerol-induced acute renal failure in the rat.

作者信息

Wolfert A I, Oken D E

机构信息

Department of Medicine, Medical College of Virginia, Richmond 23298-0160.

出版信息

J Clin Invest. 1989 Dec;84(6):1967-73. doi: 10.1172/JCI114386.

Abstract

The glomerular dynamic correlates of failed filtration were studied in volume replete rats with established glycerol-induced acute renal failure (ARF). Over one-half of all nephrons formed virtually no filtrate, while the single nephron glomerular filtration rate (SNGFR) of fluid-filled nephrons, measured at the glomerulotubular junction to preclude the possibility of covert tubular leakage, averaged one-sixth of control (P less than 0.001). Even that low mean value was elevated by a few nephrons with a near normal SNGFR. Renal failure thus reflected both total filtration failure in the majority of nephrons and massively reduced filtration in most of the remainder. Glomerular capillary pressure (Pg) averaged some 14 mmHg below control (P less than 0.001), whereas the arterial colloid osmotic and Bowman's space pressures were not significantly altered. Renocortical and whole kidney blood flow were also unchanged. Marked internephron functional heterogeneity precluded estimates of the ultrafiltration coefficient. However, the fall in SNGFR correlated well with the markedly depressed Pg and afferent net filtration pressure (delta PnetA, P less than 0.001), which in turn were caused by increased preglomerular resistance and a reciprocal fall in efferent arteriolar resistance. This complex change in intrarenal resistances was largely, if not entirely, responsible for failed filtration in this ARF model.

摘要

在容量充足且已建立甘油诱导的急性肾衰竭(ARF)的大鼠中,研究了滤过功能衰竭的肾小球动力学相关因素。超过一半的肾单位几乎不形成滤液,而在肾小球肾小管交界处测量的充盈液体的肾单位的单肾单位肾小球滤过率(SNGFR),以排除隐蔽性肾小管漏出的可能性,平均为对照组的六分之一(P<0.001)。即使是那个低的平均值也被一些SNGFR接近正常的肾单位所提高。因此,肾衰竭既反映了大多数肾单位的完全滤过功能衰竭,也反映了其余大多数肾单位的滤过功能大幅降低。肾小球毛细血管压力(Pg)平均比对照组低约14 mmHg(P<0.001),而动脉胶体渗透压和鲍曼间隙压力没有明显改变。肾皮质和全肾血流量也没有变化。明显的肾单位间功能异质性使得超滤系数的估计变得困难。然而,SNGFR的下降与显著降低的Pg和入球净滤过压(ΔPnetA,P<0.001)密切相关,而这又依次是由肾小球前阻力增加和出球小动脉阻力的相应下降引起的。肾内阻力的这种复杂变化在很大程度上(如果不是完全的话)导致了这个ARF模型中的滤过功能衰竭。

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