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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antihistaminics of various chemical structures: chlorcyclizine, chloropyramine, chlorpheniramine, clemastine, diphenhydramine, mepyramine, promethazine, and thenalidine were investigated for the action in tests for antidepressant drugs. The antihistaminics did not affect significantly the spontaneous locomotor activity of rats. Most of them (chloropyramine, chlorpheniramine, diphenhydramine, promethazine and thenalidine) increased amphetamine hypermotility but chlorcyclizine significantly inhibited, and clemastine and mepyramine did not affect it. In mice, chlorcyclizine, mepyramine and promethazine inhibited amphetamine hypermotility, while others antihistaminics were without effect. L-DOPA-induced hypermotility in mice was inhibited by all compounds tested. With the exception of chlorpheniramine and mepyramine, all tested antihistaminics produced hypothermia in mice, although fife of them (chlorpheniramine, diphenhydramine, chlorcyclizine, chloropyramine and thenalidine) antagonized the reserpine-induced hypothermia. With the exception of mepyramine and clemastine, the compounds tested shortened the period of immobility of rats in the behavioral despair test. The results indicate that only few antihistaminics have pharmacological profile resembling tricyclic or atypical antidepressant drugs.
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PMID:Effects of antihistaminic drugs in tests for antidepressant action. 611 82

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

Effects of three phosphodiesterase (PDE) inhibitors (rolipram, IBMX, and Ro 20-1724) were studied in mice in some tests predictive for antidepressant activity. All the drugs antagonized reserpine-induced hypothermia and slightly antagonized reserpine-evoked hypoactivity. Rolipram and IBMX were also effective in behavioral despair test. On the other hand, the examined PDE inhibitors did not affect apomorphine-induced hypothermia and did not potentiate the central action of L-DOPA. These results show that psychopharmacological profile of the PDE inhibitors differs from that of classical imipramine-like antidepressants.
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PMID:Antidepressant properties of some phosphodiesterase inhibitors. 619 18

2-Bromolisuride (2-Br-LIS), a derivative of the ergot dopamine (DA) agonist lisuride, was investigated in rodents in comparison with the DA antagonist haloperidol with regard to its influence on DA related behaviour, cerebral DA metabolism and prolactin (PRL) secretion. 2-Br-LIS produced catalepsy in mice (ED50 3.3 mg/kg i.p.), antagonized apomorphine-induced stereotypies in mice (ED50 0.4 mg/kg i.p.), antagonized DA agonist-induced stereotypies in rats (0.1-1.56 mg/kg i.p.), inhibited locomotor activity in rats (0.025-6.25 mg/kg i.p.), antagonized the hyperactivity produced by various DA agonists in rats (0.025-6.25 mg/kg i.p.) and inhibited the apomorphine-induced hypothermia in mice (0.05-0.78 mg/kg i.p.). 2-Br-LIS (0.03-10 mg/kg i.p.) stimulated DA biosynthesis and DOPAC formation in the striatum and DA rich limbic system of rats, but had no effect on serotonin turnover. In striatum and limbic forebrain of gamma-butyrolactone-pretreated rats 2-Br-LIS reversed the apomorphine-induced inhibition of DOPA accumulation. 2-Br-LIS (0.03 - 3 mg/kg) enhanced PRL secretion in intact male rats. These findings indicate DA antagonistic properties of 2-Br-LIS presumably due to blockade of central pre- and postsynaptic DA receptors being of approximately the same order of potency as haloperidol. 2-Br-LIS is the first ergot compound with definite antidopaminergic properties suggesting its potential usefulness as a neuroleptic.
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PMID:Central antidopaminergic properties of 2-bromolisuride, an analogue of the ergot dopamine agonist lisuride. 660 92

Mice were pretreated once daily with L-DOPA (200 mg/kg) plus benserazide (B) (50 mg/kg) for ten days and challenged with various doses of L-DOPA + B on the first, fourth or sixteenth days of withdrawal. L-DOPA + B-pretreated mice were more sensitive the locomotor stimulant effect of L-DOPA + B challenge one and four days, but not sixteen days after withdrawal. The enhanced response was most marked on the first day of withdrawal. Other mice, pretreated once daily with B (50 mg/kg), responded one day after the tenth dose with a slightly enhanced response to L-DOPA + B challenge compared to the response to vehicle-pretreated animals. Moreover, vehicle-pretreated mice challenged with B alone, were significantly less active than those challenged with vehicle. On the first day of withdrawal, the L-DOPA + B-pretreated animals were supersensitive to locomotor stimulant effects of apomorphine but subsensitive to dexamphetamine (Bailey et al., 1979). On the fourth day of withdrawal, there were no differences in the responses of the L-DOPA + B-pretreated mice compared to the vehicle-pretreated mice, to apomorphine or apomorphine plus clonidine, but L-DOPA + B-pretreated mice were still subsensitive to the locomotor stimulant effects of dexamphetamine. Clonidine produced a dose-dependent, but similar, degree of hypothermia in both pretreatment groups. On the first and fourth days of withdrawal L-DOPA + B-pretreated mice exhibited higher brain levels of dopamine (DA) and DOPA than vehicle-pretreated mice in response to an acute dose of L-DOPA + B. The biochemical results suggest that the enhanced locomotor response to L-DOPA + B in L-DOPA + B-pretreated mice is probably dependent on changes in the amount of L-DOPA (and DA) available in the brain. Moreover, it is not ruled out that some of the effects of L-DOPA + B pretreatment were due to the B alone. Some of the enhanced response to L-DOPA + B on the first day of withdrawal may have been dependent on the same mechanism as that underlying the apparent supersensitivity to apomorphine. The subsensitive response to dexamphetamine would appear to be independent of changes in post-synaptic DA and alpha-adrenergic receptor sensitivity.
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PMID:Chronic L-DOPA treatment of mice: a behavioural and biochemical study. 678 71

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 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

The effects of catecholamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) on the thermoregulatory responses of conscious rabbits to different ambient temperatures (Ta) (2, 22, and 30 degrees C) were assessed. Intravenous administration of L-DOPA alone, intravenous administration of L-DOPA plus R04-4602 (a peripheral decarboxylase inhibitor), and intraventricular administration of L-DOPA or norepinephrine all produced a hypothermia at Ta 2 degrees C. The hypothermia was due to a decrease in metabolic heat production (M). On the other hand, L-DOPA or norepinephrine produced both behavioral excitation and hyperthermia at both Ta 22 and 32 degrees C. At Ta 22 degrees C, the hyperthermia was due to decreased ear skin blood flow (EBF) and slightly increased M (due to behavioral excitation) whereas at Ta 32 degrees C the hyperthermia was due to EBF, decreased respiratory evaporative heat loss, and slightly increased M (due to behavioral excitation). Further, the temperature effects induced by L-DOPA were antagonized by pretreatment with 6-hydroxydopamine (a relative depletor of catecholaminergic nerve fibers) but not with haloperidol (a relative blocker of dopaminergic receptors). The data indicate that activation of central adrenergic receptors via the endogeneous release of norepinephrine with L-DOPA inhibits both heat production and heat loss mechanisms in the rabbit.
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PMID:The catecholamine precursor L-3,4-dihydroxyphenylalanine inhibits both heat production and heat loss mechanisms in the rabbit. 722 33

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

Exposure (2 h) of male albino rats to higher environmental temperature (HET, 40 degrees C) significantly increased the body temperature (BT). Administration of bicuculline (1 mg/kg, i.p.), physostigmine (0.2 mg/kg, i.p.), or their combination significantly raised the BT of normal rats (kept at 28 degrees C) or of HET-exposed rats. Atropine (5 mg/kg, i.p.) abolished the hyperthermic effect of bicuculline in normal and HET-exposed rats. The BT of normal and HET-exposed rat was increased with morphine (1 mg/kg, i.p.) and was reduced with naloxone (1 mg/kg, i.p.). Bicuculline or physostigmine-induced rise in BT of HET-exposed rats was potentiated following cotreatment of physostigmine with morphine. Atropine-induced hypothermia was abolished due to the cotreatment of atropine with morphine with physostigmine but was attenuated with atropine. In normal rats (kept at 28 degrees C), only atropine attenuated (morphine + bicuculline)-induced hyperthermia. L-Dopa + carbidopa or haloperidol did not significantly affect the BT of rats under similar conditions. These results suggest that short-term (2 h) exposure to HET activates the opioidergic neuron, which activates cholinergic activity through the inhibition of GABAergic system and, thus, enhances the BT.
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PMID:Higher environmental temperature-induced increase of body temperature: involvement of central opioidergic-GABAergic interaction. 750 82


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