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大鼠半乳糖胺诱导的肝衰竭中的局部脑水肿和氯化物间隙

Regional cerebral edema and chloride space in galactosamine-induced liver failure in rats.

作者信息

Gove C D, Hughes R D, Ede R J, Williams R

机构信息

Institute of Liver Studies, King's College School of Medicine and Dentistry, London, England.

出版信息

Hepatology. 1997 Feb;25(2):295-301. doi: 10.1002/hep.510250207.

Abstract

The pathogenesis of cerebral edema, which is a major complication of fulminant hepatic failure, is poorly understood. In previous studies, increased regional brain water content was observed in rats at an early stage of acute liver failure caused by galactosamine. At a later stage when the animals had developed deep coma, brain water content was reduced, possibly as a result of generalized dehydration. In the present investigation, we have determined brain water content at a late stage of liver failure, 48 hours after galactosamine, in animals that had been maintained in fluid balance by continuous intraperitoneal infusion of glucose solution. In these animals, brain water content, determined from the ratio of wet to dry weight, showed a greater increase than that observed previously at the early stage (hindbrain region [cerebellum, pons, and brain stem] increased by 4.2%; forebrain region increased by 1.4% compared with controls). Regional analysis of brain water, using a tissue-specific gravity method, showed a significant increase in cerebellar gray matter water content. Analysis of chloride space showed the extra fluid to be mainly extracellular in the hindbrain region, but not in the forebrain region. Ultrastructural examination of capillaries in gray matter from cerebellum and cerebrum showed no evidence of gross disruption of the tight junctions. Swelling of the astroglial foot processes was observed in the cerebellar gray matter. These results suggest that both vasogenic and cytotoxic mechanisms of edema formation occur in the brain during liver failure.

摘要

脑水肿是暴发性肝衰竭的主要并发症,其发病机制尚不清楚。在先前的研究中,在由半乳糖胺引起的急性肝衰竭早期,大鼠的局部脑含水量增加。在后期动物出现深度昏迷时,脑含水量降低,这可能是全身脱水的结果。在本研究中,我们测定了在半乳糖胺处理48小时后肝衰竭晚期动物的脑含水量,这些动物通过持续腹腔输注葡萄糖溶液维持了液体平衡。在这些动物中,通过湿重与干重之比测定的脑含水量比先前在早期观察到的增加幅度更大(后脑区域[小脑、脑桥和脑干]增加了4.2%;与对照组相比,前脑区域增加了1.4%)。使用组织比重法对脑含水量进行区域分析,结果显示小脑灰质含水量显著增加。氯化物空间分析表明,后脑区域额外的液体主要存在于细胞外,但前脑区域并非如此。对小脑和大脑灰质中的毛细血管进行超微结构检查,未发现紧密连接有明显破坏的证据。在小脑灰质中观察到星形胶质细胞足突肿胀。这些结果表明,肝衰竭期间脑内会发生血管源性和细胞毒性水肿形成机制。

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