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硝酸铀酰诱导的大鼠急性肾衰竭中的肾小球内皮细胞

Glomerular endothelial cells in uranyl nitrate-induced acute renal failure in rats.

作者信息

Avasthi P S, Evan A P, Hay D

出版信息

J Clin Invest. 1980 Jan;65(1):121-7. doi: 10.1172/JCI109641.

Abstract

In uranyl nitrate (UN)-induced acute renal failure (ARF) glomerular ultrafiltration coefficient (K(f)) decreases because of unknown reasons. Since transport of water across the glomerular capillary wall occurs predominantly extracellularly through the endothelial fenestrae (EF), a reduction in the diameter and/or the density of EF can reduce the extracellular filtration area and the glomerular K(f). To examine this possibility, ARF was induced in rats by intravenous administration of UN in low (15 mg/kg) and high doses (25 mg/kg). Fenestral density ( x+/-SEM) per 5 cm(2) from the scanning electron micrographs (x30,000) was 107+/-10, 103+/-9, and 101+/-11 at 2, 7, and 17 h after the intravenous administration of bicarbonate saline to the control rats. In the low-dose UN group the EF density was 91+/-2, 52+/-8, and 45+/-11 at 2, 7, and 17 h after the injection, whereas for the high-dose group at corresponding time intervals the EF density was 95+/-3, 54+/-9, and 44+/-10. Fenestral diameters, in Angstrom units ( x+/-SEM), were 751+/-53, 765+/-43, and 764+/-37 at 2, 7, and 17 h after the injection of bicarbonate saline to control rats. At corresponding intervals after the administration of UN, the fenestral diameters were 501+/-61, 472+/-28, and 438+/-98 for the low-dose group and 525+/-43, 470+/-39, and 440+/-56 for the high-dose group. 2, 7, and 17 h after the injection of UN, fenestral area of the low-dose group decreased to 52.1, 30.1, and 24.6% of the controls, whereas in the high-dose group, the fenestral area declined to 54.3, 30.2, and 23.6% of the controls. Administration of UN (15 mg/kg) to sodium-loaded rats did not alter renal function or endothelial cell morphology. It is suggested that in UN-induced ARF the morphological alterations in endothelial cells reduce the K(f) of glomerular capillaries by reducing the filtration area.

摘要

在硝酸铀酰(UN)诱导的急性肾衰竭(ARF)中,肾小球超滤系数(K(f))因不明原因而降低。由于水穿过肾小球毛细血管壁的转运主要通过内皮窗孔(EF)在细胞外发生,EF直径和/或密度的减小会减少细胞外滤过面积和肾小球K(f)。为了检验这种可能性,通过静脉注射低剂量(15 mg/kg)和高剂量(25 mg/kg)的UN诱导大鼠发生ARF。对照大鼠静脉注射碳酸氢盐生理盐水后2、7和17小时,扫描电子显微镜图像(放大30,000倍)中每5 cm²的窗孔密度(x±SEM)分别为107±10、103±9和101±11。在低剂量UN组中,注射后2、7和17小时的EF密度分别为91±2、52±8和45±11,而高剂量组在相应时间间隔的EF密度为95±3、54±9和44±10。对照大鼠注射碳酸氢盐生理盐水后2、7和17小时,窗孔直径(单位为埃,x±SEM)分别为751±53、765±43和764±37。在注射UN后的相应间隔时间,低剂量组的窗孔直径分别为501±61、472±28和438±98,高剂量组为525±43、470±39和440±56。注射UN后2、7和17小时,低剂量组的窗孔面积降至对照组的52.1%、30.1%和24.6%,而高剂量组的窗孔面积降至对照组的54.3%、30.2%和23.6%。给钠负荷大鼠注射UN(15 mg/kg)不会改变肾功能或内皮细胞形态。提示在UN诱导的ARF中,内皮细胞的形态改变通过减小滤过面积降低了肾小球毛细血管的K(f)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d22/371346/348cf66b022f/jcinvest00685-0131-a.jpg

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