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甘油诱导的急性肾衰竭的机制。

The mechanism of glycerol-induced acute renal failure.

作者信息

Hobbs J B, Chusilp S, Kincaid-Smith P, McIver M A

出版信息

J Lab Clin Med. 1976 Jul;88(1):44-53.

PMID:778314
Abstract

Ten rabbits with transparent ear chambers were grafted with small pieces of kidney. The resulting vessel anastomosis and restoration of renal blood flow allowed continuous microscopic observations of functioning renal tissue in vivo. When the grafts were well established, acute renal failure was induced in the rabbit by glycerol injection. All cases showed similar changes. Within minutes the brisk blood flow within the renal grafts became progressively more sluggish until complete stasis was established. The initial change was a blanching of intertubular and glomerular capillaries with progressive dilation and stasis of renal veins. Only after almost complete cessation of blood flow in most graft vessels, generally after a further 10 minutes, was any change in arteries or arterioles observed. The afferent arterioles and then larger arteries showed constriction followed by complete stasis. The ear chamber vessels (nonrenal) continued to flow normally. Blood flow was slowly re-established in the grafts and by the next day was normal in the surviving rabbits. These studies provided visual in vivo evidence that the mechanism of glycerol-induced acute renal failure is mediated by a reversible renal ischemia and that the factors responsible act particularly on renal vasculature. However, the mechanism whereby blood flow ceases is obscure and it cannot be attributed to arterial or arteriolar constriction.

摘要

十只带有透明耳室的兔子被移植了小块肾脏。由此产生的血管吻合以及肾血流的恢复使得能够在体内对正常运作的肾组织进行连续的显微镜观察。当移植组织稳固建立后,通过注射甘油在兔子身上诱发急性肾衰竭。所有病例都表现出相似的变化。数分钟内,肾移植组织内原本活跃的血流逐渐变得更加迟缓,直至完全停滞。最初的变化是肾小管间和肾小球毛细血管变白,肾静脉逐渐扩张并出现血流停滞。通常在大多数移植血管的血流几乎完全停止之后,再过10分钟左右,才观察到动脉或小动脉有任何变化。入球小动脉,随后是较大的动脉,先是出现收缩,接着完全停滞。耳室血管(非肾血管)继续正常流动。移植组织中的血流缓慢恢复,到第二天,存活兔子的血流恢复正常。这些研究提供了体内可视化证据,表明甘油诱发急性肾衰竭的机制是由可逆性肾缺血介导的,且相关因素尤其作用于肾血管系统。然而,血流停止的机制尚不清楚,且不能归因于动脉或小动脉的收缩。

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