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)

1. Intraperitoneal injection of graded doses of ketamine produced a dose-dependent fall in body temperature of rats. Similarly, intracerebral injection of much smaller doses produced hypothermia.2. Pretreatment of the rats with p-chlorophenylalanine (PCPA) greatly attenuated the hypothermic response to ketamine whereas the intraperitoneal injection of 5-hydroxytryptophan in PCPA-treated rats restored the hypothermic effect of ketamine.3. Depletion of the brain monoamines by reserpine completely prevented the ketamine-induced hypothermia. Treatment with sodium diethyldithiocarbamate (DEDTC), however, did not modify the hypothermic effect of ketamine.4. Pretreatment of the rats with pargyline potentiated the ketamine-induced hypothermia.5. Depletion of brain monoamines by reserpine in combination with inhibition of noradrenaline biosynthesis (DEDTC) resulted in a long lasting fall in temperature which was not modified by ketamine.6. When the ambient temperature was raised from 26 degrees C to 32 degrees C, ketamine-induced hypothermia was much reduced and superimposed on a hyperthermia which occurred in all animals.7. It is concluded that ketamine produces hypothermia in rats possibly through the release of 5-hydroxytryptamine in the hypothalamus and that this effect is similar in some respects to that produced by morphine in non-tolerant rats.
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PMID:Role of 5-hydroxytryptamine in ketamine-induced hypothermia in the rat. 427 91

It has been suggested that hypothermia induced in rabbits by As2O3 3 mg/kg (i.v.) depends mostly on the blocking of the thermo-regulatory center. The relationship between hypothermia induced by As2O3 and brain monoamine levels in rabbits was investigated. To clarify the mechanism of the hypothermia, the influence of pretreatment with several agents on As2O3-induced hypothermia and on monoamine levels in the hypothalamus was examined. The core temperature was measured by inserting the thermister probe into the rectum and noradrenaline(NA), 5-hydroxytryptamine(5-HT) and 5-hydroxyindoleacetic acid(5-HIAA) levels in the hypothalamus were estimated fluorometrically. Pretreatment with p-chlorophenylalanine(PCPA), alpha-methyl-p-tyrosine(alpha-MPT) or 5-hydroxytryptophan(5-HTP) did not inhibit the hypothermia induced by As2O3 but did decrease NA levels in the hypothalamus. On the contrary, pretreatment with barbital sodium, pheniprazine, 1-DOPA and 1-tyrosine significantly inhibited the hypothermia or exhibited the hyperthermia. As2O3-induced hypothermia in rabbits was followed by a decrease in NA levels and an increase in 5-HT levels in the hypothalamus. On the other hand, when the hypothermia induced by As2O3 was inhibited by pretreatment with barbital sodium, pheniprazine, 1-DOPA and 1-tyrosine, both NA and 5-HT levels in the hypothalamus were significantly increased. These results suggest that As2O3-induced hypothermia is due to a decrease in NA levels and inhibition of the hypothermia is due to an increase in NA levels, in the rabbit hypothalamus.
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PMID:[Studies on As2O3-induced rabbit hypothermia and brain monoamines (author's transl)]. 615 19

The information currently available in the literature on the effects of serotonergic drugs on thermoregulation in the avian species is very scanty. Therefore, it was the objective in this project to study the influence of 5-hydroxytryptamine (5-HT), 5-hydroxytryptophan (5-HTP), benserazide, carbidopa (Mk 486), citalopram, cyproheptadine, methysergide, xylamidine, p-chlorophenylalanine (PCPA) and lysergic acid diethylamide (LSD-25) on the rectal temperature of young chicks. 5-hydroxytryptamine (0.8 mg/kg), produced significant dose-dependent hypothermia in young chicks. Similarly, 5-HTP (16 mg/kg) profoundly lowered the rectal temperature of young chicks. The hypothermic effect of 5-HTP was potentiated by benserazide (1.25-2.5 mg/kg). Pretreatment with carbidopa (50 mg/kg) potentiated 5-HTP induced hypothermia. Citalopram (5 mg/kg) significantly potentiated hypothermia induced by 5-HT. Pretreatment with PCPA (200 mg/kg, 24 hr previously) alone resulted in hyperthermia while the hypothermic effect of 5-HTP (16 mg/kg) was antagonised by pretreatment with PCPA. Cyproheptadine (1.25 mg/kg) antagonised the hypothermic effect of 5-HT (0.1 and 0.8 mg/kg). The antagonistic effect was weak when the chicks were pretreated with larger doses of cyproheptadine (i.e. 2.5-10 mg/kg). The hypothermia induced by 5-HT (0.8 mg/kg) was antagonised by smaller doses of methysergide (0.125-1.0 mg/kg) but potentiated by larger doses of methysergide (2.0 and 4.0 mg/kg). Xylamidine (1-2 mg/kg) alone induced hyperthermia and effectively antagonised hypothermia induced by 5-HT (0.8 mg/kg). D-Lysergic acid diethylamide (2.5-10 micrograms/kg) alone induced hypothermia. The interaction between LSD and 5-HT was dose-dependent and biphasic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of some serotoninergic agents on the rectal temperature of the domestic fowl (Gallus domesticus). 624 Dec 99

The pharmacological profile of salbutamol, an agonist of beta-adrenergic receptors and a potential antidepressant drug, and its effect on the central serotonin system were studied. It was found that salbutamol either had no effect, or, at higher doses, inhibited the spontaneous activity of mice and rats; it did not influence significantly either the produced by amphetamine locomotor stimulation (in mice and rats) or amphetamine stereotype (in rats). Salbutamol while not affecting body temperature of normal mice reversed hypothermia but not ptosis induced by reserpine, and counteracted the hypothermic action of apomorphine in mice. It neither affected the spiperone-induced catalepsy nor was active in the behavioural despair test in rats. Salbutamol had no effect either, on the fenfluramine-induced hyperthermia in rabbits, on the 5-hydroxytryptophan-induced head twitch reaction in mice, on the tryptamine-induced clonic convulsions of forepaw in rats on the flexor reflex in spinal rats, or on the quipazine- or fenfluramine-induced stimulation of this reflex. The above findings indicate that the pharmacological profile of salbutamol resembles that of classical imipramine-like antidepressant drugs to a very small extent and it does not affect the central serotonergic transmission.
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PMID:The central action of salbutamol, a beta-agonist with a potential antidepressant activity. 626 86

Sertraline [1S,4S-N-methyl-4-(3,4-dichlorophenyl)-1,2,3,4-tetrahydro-1-naphthylamine] was found to be a highly selective and potent competitive inhibitor of synaptosomal serotonin uptake. Sertraline also selectively reduced ex vivo uptake of serotonin and strongly antagonized the serotonin-depleting action of p-chloroamphetamine, indicating potent blockade of serotonin uptake in vivo. Acute and repeated dosing of sertraline decreased serotonin content of whole blood. Sertraline only weakly inhibited rat heart uptake of i.v. [3H]norepinephrine. In substantiation of selective blockade of serotonin uptake, sertraline potentiated various symptoms of 5-hydroxytryptophan but did not reverse reserpine-induced hypothermia. Sertraline was a very weak inhibitor of [3H]quinuclidinyl benzilate binding to rat brain membranes in vitro and did not produce anticholinergic effects in mice in vivo. Sertraline was well tolerated in mice, rats and dogs, with no locomotor stimulant effects in rats or untoward cardiovascular effects in dogs. The major metabolite, N-demethylsertraline, was also a selective serotonin uptake blocker. Sertraline strongly reduced immobility of mice in the Porsolt swim test for antidepressants. After repeated dosing in rats, sertraline diminished the cyclic AMP response of limbic forebrain adenylate cyclase to norepinephrine, as well as the binding of [3H]dihydroalprenolol to cortical membranes. It is proposed that selective blockade of serotonin reuptake can induce activation of norepinephrine neurons and subsequent down-regulation of norepinephrine receptors and that sertraline, a highly selective inhibitor of serotonin uptake, may be an efficacious antidepressant without anticholinergic or cardiovascular side-effects.
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PMID:Sertraline, 1S,4S-N-methyl-4-(3,4-dichlorophenyl)-1,2,3,4-tetrahydro-1-naphthylamine, a new uptake inhibitor with selectivity for serotonin. 631 78

A series of 5-aryl-2,3,5,6-tetrahydroimidazo[2,1-a]isoquinolin-5-ols was prepared and evaluated for potential antidepressant activity in the reserpine-induced hypothermia model and selected central nervous system and autonomic activity tests. Several members of the series, notably the 4-chloro- and 4-fluorophenyl analogues, demonstrated pharmacological activity in the range of imipramine. Both compounds provided a marked potentiation of the 5-hydroxytryptophan-facilitated monosynaptic spike in the spinal cat preparation.
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PMID:Antidepressant activity of 5-aryl-2,3,5,6-tetrahydroimidazo[2,1-a]isoquinolin-5-ols. 684 18

Pirenzepine, (5,11-dihydro-11-[(4-methylpiperazin-1-yl)-acetyl]-6H-pyrido-[2,3] [1,4]-benzodiazepin-6-one dihydrochloride), tested on rats and mice, did not demonstrate any conspicuous behavioral action: it did not counteract reserpine hypothermia in mice, the L-DOPA hypermotility of mice, and (with the exception of very large doses) the amphetamine hypermotility in mice and rats. The drug neither prolonged the time of immobility of rats in the behavioral despair test, nor affected the central serotonin system in rats in tests for 5-hydroxytryptophan-induced head twitches, tryptamine-induced convulsions and fenfluramine-induced hyperthermia at high ambient temperature. Pirenzepine did not affect either the hind limb flexor reflex in the spinal rat, nor the action of serotoninomimetics of it. The investigated compound had strong peripheral cholinolytic action as it inhibited salivation and lacrimation in the oxotremorine test. The oxotremorine tremor was weakened only by very high doses of pirenzepine. LD50 of the drug in mice was 412 mg/kg ip.
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PMID:Central action of pirenzepine. 689 18

A dose of 40 mg/kg of meperidine (pethidine) caused a marked lowering of rectal temperature in restrained female rats at room temperature (22 degrees C). This decrease was not antagonized by injection of 1 mg/kg of naloxone, whereas hypothermia of equal magnitude induced by 20 mg/kg of morphine was reversed by 1 mg/kg of naloxone. Pretreatment with the serotonin reuptake blocker, fluoxetine (10 mg/kg), or a non-hypothermic dose of meperidine (20 mg/kg) significantly potentiated the hypothermia induced by 100 mg/kg of l-5-hydroxytryptophan. The hypothermic effect of 40 mg/kg of meperidine was significantly greater than that of 10 mg/kg of fluoxetine. Finally, 40 mg/kg of meperidine produced a significantly greater hypothermic effect in restrained rats than in unrestrained rats. The results indicate that the hypothermic effect of meperidine is not a result of an opioid action, and that although it may be mediated through serotonergic systems, inhibition of serotonin reuptake is probably not the primary mechanism.
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PMID:Meperidine-induced hypothermia in the rat. 698 42

A psychopharmacological profile of mesterolone, an androgen and potential antidepressant drug, was tested in mice and rats. Given in a dose of 80 mg/kg ip, mesterolone potentiated the action of L-DOPA in mice and in doses 40 and 80 mg/kg ip potentiated the amphetamine stereotypy in rats. On the other hand, in doses of 20--80 mg/kg ip mesterolone did not affect the reserpine induced hypothermia and ptosis, did not antagonize the apomorphine induced hypothermia in mice, did not change the motor stimulation produced by amphetamine and did not affect the spiperone induced catalepsy in rats. Mesterolone did not affect the head twitch response after 5-hydroxytryptophan in mice and was inactive in the behavioral despair test in rats. The results indicate that the psychopharmacological profile of mesterolone only slightly resembles the profile of classical imipramine-like anti-depressants.
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PMID:Psychopharmacological profile of mesterolone. 719 78

Ketotifen (4-/1-methyl-4-piperidylidene/-4H-benzo[4,5]cyclohepta[1,2-b]thiophen-10(9H)-one hydrogen fumarate) inhibited spontaneous locomotor activity and amphetamine hypermotility in mice and rats, as well as L-DOPA-induced motor stimulation in mice. It produced in mice a slight hypothermia and did not prevent reserpine-induced hypothermia; thus, it does not posses properties or tricyclic antidepressants. Ketotifen showed some features of serotoninolytic: it inhibited the head twitch response to 5-hydroxytryptophan in mice, depressed tryptamine-induced clonic convulsions in rats, antagonized fenfluramine-induced hyperthermia in rats at high ambient temperature and showed weak antiserotonin action in the flexor reflex preparation. Ketotifen did not affect spiperone- or reserpine-induced catalepsy and showed no cholinolytic activity. LD50 of ketotifen (after 24 h) was 122.5 mg/kg ip in mice and 62.6 mg/kg ip in rats.
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PMID:Central action of ketotifen. 733 54


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