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)

Chlorpromazine- and haloperidol-induced hypothermia were examined in mice. The alpha 1 receptor agonist phenylephrine partially antagonized the hypothermia, while the dopamine D2 receptor agonist apomorphine did not inhibit it. The central serotonin2 (5-HT2) receptor agonist I-2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) strongly inhibited the chlorpromazine- and haloperidol-induced hypothermia. Both drugs at doses which can elicit hypothermia antagonized head twitch responses mediated by the central 5-HT2 receptor. These results suggest that the chlorpromazine- and haloperidol-induced hypothermia may be mediated by the blockade of the central 5-HT2 receptor.
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PMID:Serotonin2 (5-HT2) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) inhibits chlorpromazine- and haloperidol-induced hypothermia in mice. 859 84

We report herein the findings of a 2-year-old boy in whom junctional tachycardia developed 2 days after he underwent a modified Fontan operation and thereafter was successfully treated by hypothermia without paralyzing and artificially ventilating the patient. Chlorpromazine was useful in achieving moderate hypothermia by surface cooling without producing any unfavorable effects associated with topical cooling.
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PMID:Successful management of junctional tachycardia by hypothermia after a Fontan operation. 869 35

Effects of prolonged lithium administration was seen on the action of various psychoactive drugs in animals. Apomorphine induced pecking in pigeons increased significantly by lithium treatment for 14 days, from 1445.3 +/- 202.5 in control to 2785.8 +/- 205.8 in Gp. B. Haloperidol-induced catalepsy score in albino rats increased significantly following chronic lithium treatment compared to control. Chlorpromazine-induced hypothermia in rabbits was immediate but transient, while in lithium treated rabbits induction of hypothermia was delayed, sustained and of greater magnitude. This action of lithium may be mediated by increasing the permeability of blood-brain barrier, or enhancing the sensitivity of alpha-adrenoceptors in brain.
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PMID:Effects of oral lithium on the action of various C.N.S. active drugs. 895 Jan 40

We investigated micronucleus induction in rats treated with chlorpromazine and reserpine, drugs that induce hypothermia. We administered chlorpromazine (31.3--250mg/kg) or reserpine (500--2000 mg/kg) intraperitoneally and measured temperature rectally. Chlorpromazine at 62.5-250mg/kg and reserpine at all doses significantly decreased rectal temperature, although the hypothermic response was weaker than previously reported in mice. Only chlorpromazine at 250mg/kg decreased rectal temperature transiently to <33 degrees C for 20h and induced a statistically significant increase in micronucleated polychromatic erythrocyte frequency. When rats treated with reserpine at 500mg/kg were exposed to an environmental temperature of 16 degrees C for 6, 12, or 24h to keep their body temperature under 33 degrees C, only the 24h treatment group significantly induced micronuclei. In addition, relatively large micronuclei (diameter of micronucleus> or = 1/4 diameter of cytoplasm) accounted for 33.0% of the induced micronuclei, suggesting that hypothermia affected the mitotic apparatus. The hypothermic response to chlorpromazine and reserpine was weaker in rats than in mice, and it was correspondingly more difficult to induce micronuclei in rats with those drugs.
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PMID:Effects of chemically- and environmentally-induced hypothermia on micronucleus induction in rats. 1108 Jun 63

Chlorpromazine induces in rats a marked and long-lasting hyperglycaemia which (a) is more marked at low than high room temperatures, (b) is inhibited by phentolamine but not by dibenamine, and (c) is prevented by adrenalectomy, by removal of the adrenal medullae and by treatment of the rats with reserpine. Other experimental results suggest that there is a correlation between the hyperglycaemia and the hypothermia induced by chlorpromazine and by its congeners. The hyperglycaemia seems to be the result of at least two factors: an activation of the adrenergic mechanisms and an impaired peripheral utilization of glucose.
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PMID:STUDIES ON THE HYPERGLYCAEMIA INDUCED BY CHLORPROMAZINE IN RATS. 1420 96

The effects of chlorpromazine-treatment timing on the development of the placenta in pregnant rats were examined. Chlorpromazine was administered intraperitoneally at 100mg/kg on gestation day (GD) 11 (GD11-treated group), GD 13 (GD13-treated group) or GD 15 (GD15-treated group) into pregnant rats. All treated dams exhibited decreased body weight, prone position, hypothermia, loss or decrease of locomotor activity, etc. The fetal mortality rates were increased up to 42.9% in the GD11- and GD13-treated groups and up to 16.7% in the GD15-treated group. The embryo/fetal weight was on a declining trend from GD 16 onward, and the intrauterine growth retardation (IUGR) rates on GD 21 were increased in all treated groups. The placental weight showed a declining trend from GD 15 onward in all treated groups. Histopathologically, apoptosis was detected 1 or 2 days after treatment, and led to hypoplasia in the labyrinth zone and metrial gland, and cystic degeneration in the basal zone on GD 21 in all treated groups. There was no difference in the histopathological lesions on GD 21 among the treated groups. Thus, it is considered that chlorpromazine-induced placental toxicity is characterized in that there is no obvious specific sensitive period from GD 11 to GD 15. Chlorpromazine induced a non-specific transient development retardation of the placenta by apoptosis independently of the cell proliferation period in each part/zone.
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PMID:Histomorphological comparison of rat placentas by different timing of chlorpromazine-administration. 2619 76


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