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抑制性神经调质不会改变实验性肝性脑病的病程。

Inhibitory neuromodulators do not alter the course of experimental hepatic encephalopathy.

作者信息

Rzepczynski D, Zieve L, Lindblad S

机构信息

VA Medical Center, Minneapolis, Minnesota.

出版信息

Metab Brain Dis. 1988 Sep;3(3):211-6. doi: 10.1007/BF00999237.

Abstract

The neuromodulators, adenosine, serotonin, and glycine, did not alter the course of hepatic encephalopathy (HE) that followed a portacaval shunt and hepatic artery ligation in rats. The substances were instilled into the brain ventricle through an intraventricular cannula in doses that affect other aspects of behavior in the normal rat (adenosine, suppression of food intake; serotonin, loss of muscle strength and ataxia; glycine, leaning and circling). A subconvulsive dose of the glycine antagonist, strychnine, also had no effect on the course of HE. A large dose of the adenosine antagonist, caffeine, had a depressive rather than excitatory effect and shortened the time taken to induction of coma. These studies and a similar previous one with gamma-aminobutyric acid (GABA) suggest that the inhibitory neuromodulators do not have a prominent role in the pathogenesis of hepatic coma.

摘要

神经调质腺苷、5-羟色胺和甘氨酸,不会改变大鼠门腔静脉分流术和肝动脉结扎术后肝性脑病(HE)的病程。这些物质通过脑室内插管注入脑室,剂量足以影响正常大鼠行为的其他方面(腺苷,抑制食物摄入;5-羟色胺,肌肉力量丧失和共济失调;甘氨酸,倾斜和转圈)。亚惊厥剂量的甘氨酸拮抗剂士的宁,对HE病程也无影响。大剂量的腺苷拮抗剂咖啡因具有抑制而非兴奋作用,并缩短了诱导昏迷所需的时间。这些研究以及先前一项关于γ-氨基丁酸(GABA)的类似研究表明,抑制性神经调质在肝昏迷的发病机制中并不起主要作用。

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