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韦尼克脑病模型。

Model of Wernicke's encephalopathy.

作者信息

Troncoso J C, Johnston M V, Hess K M, Griffin J W, Price D L

出版信息

Arch Neurol. 1981 Jun;38(6):350-4. doi: 10.1001/archneur.1981.00510060052007.

Abstract

After a week on a thiamine-free diet and daily injections of pyrithiamine hydrobromide, a group of rats began to lose weight; soon thereafter hypothermia, piloerection, and ataxia developed, followed by convulsions and death. Neuropathologic examination disclosed hemorrhagic necrotic lesions in the thalamus, hypothalamus, collicular plate, vestibular nuclei, and inferior olives. The control groups did not show neurologic signs or neuropathologic abnormalities. The lesions in thiamine-deficient rats were similar in character and distribution to those of human Wernicke's disease. Because this experimental regimen produces neuropathologic changes rapidly and consistently, this animal model should be useful in studies designed to examine the pathophysiologic aspects of experimental Wernicke's disease in particular and CNS thiamine deficiency in general.

摘要

在一周无硫胺饮食并每日注射氢溴酸吡硫胺后,一组大鼠开始体重减轻;此后不久出现体温过低、竖毛和共济失调,随后发生惊厥和死亡。神经病理学检查发现丘脑、下丘脑、丘状板、前庭核和下橄榄核有出血性坏死病变。对照组未出现神经体征或神经病理学异常。硫胺缺乏大鼠的病变在性质和分布上与人类韦尼克脑病相似。由于这种实验方案能迅速且持续地产生神经病理学变化,这种动物模型在旨在研究实验性韦尼克病特别是中枢神经系统硫胺缺乏的病理生理学方面的研究中应该会很有用。

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