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半乳糖胺诱导的暴发性肝炎家兔的脑水肿。区域差异及对颅内压的影响。

Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure.

作者信息

Traber P G, Ganger D R, Blei A T

出版信息

Gastroenterology. 1986 Dec;91(6):1347-56. doi: 10.1016/0016-5085(86)90186-1.

DOI:10.1016/0016-5085(86)90186-1
PMID:3770359
Abstract

Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% +/- 0.49% with significant elevations to 81.96% +/- 0.47% and 82.95% +/- 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2-9 mmHg and the range of peak values in galactosamine-treated rabbits was 18-55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.

摘要

脑水肿和颅内高压是暴发性肝衰竭的主要并发症。我们研究了半乳糖胺诱导的中毒性肝炎家兔脑水肿的发展情况并监测了其颅内压。通过重量分析法检测小组织样本,我们发现大脑皮质灰质中的脑含水量增加,但皮质下、中脑、脑桥白质以及小脑中的含水量并未增加。对照动物大脑灰质中的含水量比例为80.96%±0.49%,在轻度和重度脑病中分别显著升高至81.96%±0.47%和82.95%±1.49%。这分别对应组织体积平均增加5.5%和11.7%。在重度脑病中,海马灰质也出现积水,平均组织体积增加30%。脑含水量的区域增加通过干湿重法得到证实。不存在低血压、缺氧或严重低血糖来解释水肿现象。随着脑病的发展,通过脑室内插管对未麻醉的家兔持续监测颅内压。轻度阶段压力正常,但重度脑病动物的颅内压会间歇性升高。颅内压的正常范围是2 - 9 mmHg,半乳糖胺处理的家兔峰值范围是18 - 55 mmHg。脑含水量积聚的区域差异表明,细胞肿胀以及水通过血脑屏障的移动异常可能是该模型中脑水肿的原因。

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