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支持肾小管漏出作为汞中毒所致无尿原因的形态学证据。

Morphologic evidence to support the role of tubular leakage as a cause of anuria induced by meercury poisoning.

作者信息

Wada T, Aizawa K, Kan K, Kitamoto K, Kuroda S, Ogawa M, Kato E

出版信息

Am J Pathol. 1974 Nov;77(2):175-83.

Abstract

The qualitative Hanssen technic was used to study the mechanism of anuria produced in rabbits by mercury poisoning. Twenty-four to 30 hours after intravenous injection of a low dose of HgCl(2), the animals were almost completely anuric. Sodium ferrocyanide injected intravenously was visualized as Prussian blue in essentially all glomeruli in anuric kidneys, and the amount of the dye in the glomerular tufts was almost the same as in control kidneys. Thus there was no evidence for a severe reduction in glomerular capillary blood flow. Besides, the distribution of Prussian blue in tubular lumina indicated that the anuria occurred in the presence of a significant glomerular filtration. Tubular walls of the anuric kidneys showed an abnormally increased permeability to sodium ferrocyanide. These findings suggested that the anuria during this stage was caused more by tubular leakage than by intrarenal vasoconstriction and subsequent cessation of glomerular filtration.

摘要

采用定性的汉森技术研究汞中毒导致家兔无尿的机制。静脉注射低剂量HgCl₂后24至30小时,动物几乎完全无尿。静脉注射的亚铁氰化钠在无尿肾脏的几乎所有肾小球中都被染成普鲁士蓝,肾小球丛中的染料量与对照肾脏几乎相同。因此,没有证据表明肾小球毛细血管血流量严重减少。此外,普鲁士蓝在肾小管管腔中的分布表明,无尿是在肾小球滤过显著存在的情况下发生的。无尿肾脏的肾小管壁对亚铁氰化钠的通透性异常增加。这些发现表明,这个阶段的无尿更多是由肾小管渗漏引起的,而不是肾内血管收缩和随后肾小球滤过停止所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/005b/1910904/aa097eb58c84/amjpathol00469-0071-a.jpg

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