Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of electroconvulsive shock (ECS) on brain histamine (HI) levels, 1-histidine decarboxylase (HD) and HI-methyltransferase (HMT) activities, and H2-receptor--mediated hypothermia were studied in rats. Single (x1) and repeated (x10, once daily) ECS had practically no effect on both HI levels and HMT activities in the rat hypothalamus, cerebral cortex and rest of the brain. ECS x10 significantly increased HI accumulation. ECS x1 (only after 24 h) and ECS x10 resulted in marked elevation of the brain HD activity; the most pronounced effect was observed in the cerebral cortex. Repeated, but not single, ECS reduced the hypothermic action of various centrally given histamine H2-receptor agonists (HI, 4-methylHI, dimaprit and impromidine). It is suggested that prolonged treatment with ECS activates the central histaminergic system in the rat. The histaminergic neurons in the cerebral cortex seem to be especially affected by repeated ECS.
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PMID:Effect of electroconvulsive shock (ECS) treatment on the histaminergic system in rat brain: biochemical and behavioural studies. 372 5

The purpose of this study was to examine the effects of intracerebroventricular (i.c.v.) administration of N-acetylhistamine on rectal temperature, histamine level, histidine decarboxylase (HDC) activity, and the turnover rate of monoamines in mice. More than 60 micrograms of N-acetylhistamine induced hypothermia. The maximum effect of hypothermia was observed 20 min after administration of N-acetylhistamine (60-120 micrograms/mouse). A significant drop in rectal temperature of 3 degrees C was induced by 120 micrograms of N-acetylhistamine. Concurrent with the appearance of hypothermia, the histamine levels were increased. However, both histamine H1 and H2 antagonists did not prevent hypothermia. The i.c.v. administration of N-acetylhistamine inhibited HDC activity, but had no effect on the turnover rates of monoamines. These data confirmed that endogenous N-acetylhistamine may be a metabolite which lacks significant physiological roles, and demonstrated that exogenous N-acetylhistamine is not a good pharmacological tool for the study of the functions of the brain histaminergic system in mammals.
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PMID:Effects of intracerebroventricular administration of N-acetylhistamine on body temperature in mice. 776 May 82