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急性肾衰竭中的肾微血管系统

Renal microvasculature in acute renal failure.

作者信息

Takemura T, Matsubara O

出版信息

Bull Tokyo Med Dent Univ. 1975 Mar;22(1):9-23.

PMID:1055027
Abstract

The ranal microvasculature evidenced by intraarterial injection of silicone rubber performed in 10 cases of acute renal failure from various causes demonstrated definite reduction in filling with patchy deficit in subcapsular cortex, narrowing of preglomerular arterioles, especially at the branching from the interlobular arteries in the same area, relative increase in filling of vas afferens and efferens of juxtamedullary cortex, and of vasa recta in medulla. The same injection figures are observed in acute renal failure in dogs experimentally induced by ligation and clamping of renal arteries, and intraarterial infusion of large quantities of angiotensin II (1000 ng/kg/min). Although the etiological factors of acute renal failure are manifold and the parenchymal damage is varied as well, the vasoconstriction of preglomerular arterioles should be considered as an initial common pathway which continues in subcapsular cortex. The result of present experiments is consistent with the hypothesis that renin and angiotensin participate in the pathogenesis of acute renal failure.

摘要

对10例各种病因所致急性肾衰竭患者经动脉内注射硅橡胶后显示的肾微血管系统表明,包膜下皮质灌注明显减少,有片状缺损,肾小球前小动脉变窄,尤其是在同一区域小叶间动脉分支处,近髓质皮质的入球小动脉和出球小动脉以及髓质直小血管的灌注相对增加。在通过结扎和钳夹肾动脉以及动脉内输注大量血管紧张素II(1000 ng/kg/分钟)实验诱导的犬急性肾衰竭中也观察到相同的注射表现。尽管急性肾衰竭的病因多种多样,实质损害也各不相同,但肾小球前小动脉的血管收缩应被视为在包膜下皮质持续存在的初始共同途径。本实验结果与肾素和血管紧张素参与急性肾衰竭发病机制的假说一致。

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