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

Intrahypothalamic injection of 5-hydroxytryptamine (5-HT) caused a fall in core temperature in lightly restrained rats maintained at an ambient temperature of 17 degrees C. The hypothermia was blocked by 5-HT antagonists with a relative potency of methiothepin greater than methergoline greater than methysergide greater than cinanserin greater than cyproheptadine. The peripheral 5-HT antagonist, xylamidine, was not an antagonist, suggesting the hypothermia was of central origin. Other neurotransmitter antagonists, haloperidol, atropine, phentolamine, and propranolol failed to prevent 5-HT-induced hypothermia. This suggests that the hypothermic response to 5-HT can be used for a quantitative study of drug action at central 5-HT receptors.
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PMID:5-Hydroxytryptamine-induced hypothermia in rats as an in vivo model for the quantitative study of 5-hydroxytryptamine receptors. 611 2

The effects of clomipramine HCl (15 mg kg-1 i.p.) on behaviour, body temperature and brain amines were investigated in rats that had been chronically treated twice daily with increasing doses of delta 9-tetrahydrocannabinol (delta 9-THC, 2-6 mg kg-1 i.v.). delta 9-THC produced a biphasic change in behaviour, stimulation followed by depression, and a pronounced hypothermia. Tolerance developed rapidly to these effects of delta 9-THC. Chronic treatment with delta 9-THC reduced the levels of homovanillic acid, 5-hydroxytryptamine and noradrenaline. The level of dopamine was not altered with chronic treatment and tolerance appeared to develop to the increased levels of 5-hydroxyindoleacetic acid induced by delta 9-THC. Injection of clomipramine, 12-14 h after 2, 5 or 10 days of delta 9-THC treatment induced characteristic changes in the rats behaviour which consisted of writhes, backward kicking, wet shakes, jumps ataxia and front paw and whole body tremor. The severity of the behavioural changes appeared to be dependent on the period of delta 9-THC administration and they were not accompanied by a change in body temperature or consistent changes in brain amines or metabolites. The results indicate that physical dependence on delta 9-THC may occur since clomipramine is able to precipitate changes in behaviour, indicative on an abstinence syndrome, in rats chronically treated with delta 9-THC. It is suggested that tryptaminergic mechanisms are altered during chronic delta 9-THC treatment and that clomipramine induces the behavioural changes by interacting with an altered tryptaminergic system.
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PMID:Time-course of the effects of chronic delta 9-tetrahydrocannabinol on behaviour, body temperature, brain amines and withdrawal-like behaviour in the rat. 612 98

Well established as supposed antidepressant drugs, desipramine (1.25-5 mg/kg), nisoxetine (0.625-2.5 mg/kg) and clomipramine (1.25-5 mg/kg) but not fluoxetine (2.5-40 mg/kg) or citalopram (2.5-40 mg/kg) dose-dependently potentiated TRH (40 mg/kg)-induced hyperthermia in mice. Alpha-adrenergic blocking agents, phenoxybenzamine (20 mg/kg) and prazosin (5 mg/kg), which when given alone lowered body temperature, did not prevent the thermogenic effect of TRH but completely abolished the potentiating effect of clomipramine and almost completely antagonized the same effect of desipramine. The potentiating effect of desipramine on TRH-induced hyperthermia was also attenuated by 4 mg/kg l-propranolol but not by the same dose of d-propranolol. l-Propranolol (4 mg/kg) did not affect the potentiating effect of clomipramine. Cyproheptadine (5 mg/kg), an antagonist of 5-hydroxytryptamine receptors (which, like the alpha-adrenoceptor antagonist, produced hypothermia in normal mice) did not prevent the effects of clomipramine or desipramine. We conclude that a noradrenergic rather than a 5-hydroxytryptaminergic mechanism is involved in the potentiating effect of antidepressant drugs on TRH-induced hyperthermia. Hence, screening tests for antidepressants, which are based on the potentiation of the TRH-induced hyperthermia will always result in false negatives for antidepressants, such as citalopram, which are highly selective inhibitors of the uptake of 5-hydroxytryptamine.
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PMID:The effect of highly selective inhibitors of the uptake of noradrenaline or 5-hydroxytryptamine on TRH-induced hyperthermia in mice. 613 92

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

This research compares the effects, in mice and rats, of desmethylclomipramine (DCLOM) and clomipramine (CLOM). DCLOM antagonized the hypothermia induced in mice by reserpine or apomorphine to a much greater extent than CLOM. Reserpine ptosis in mice was depressed by DCLOM only. Similarly, only DCLOM was effective in the behavioral despair test in rats. DCLOM increased the 5-hydroxytryptamine (5-HT) pressor effect in pithed rats, but to a lesser extent than CLOM by several factors. Only DCLOM increased the noradrenaline (NA) pressor effect. The depletion of NA induced by 6-hydroxydopamine was depressed by DCLOM only. The 5-HT depletion induced by p-chloromethamphetamine was antagonized only by CLOM. The results obtained show that the noradrenergic mechanism is of prime importance in the action of DCLOM and of much more importance than in the action of CLOM.
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PMID:Comparison of the pharmacological actions of desmethylclomipramine and clomipramine. 621 80

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

p-Chlorophenylalanine (p-CPA) reduces brain 5-hydroxytryptamine (5-HT) without altering the dopamine and norepinephrine content. Morphine does not influence the 5-HT level, but partly reverses the depletion of 5-HT by p-CPA. Morphine analgesia and toxicity are not affected by p-CPA treatment. p-CPA also has no effect on acute morphine hypothermia, but after chronic treatment of 5-HT-deficient mice the dose--response curve is no longer parallel, which suggests that another mode of morphine hypothermia occurs. p-CPA diminishes morphine-induced running after acute as well as after chronic morphine administration. p-CPA treatment reduces the sensitivity to the naloxone-precipitated withdrawal reaction, but does not affect the development of physical dependence.
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PMID:The influence of p-chlorophenylalanine on different morphine effects. 644 58

Immobilization of albino rats for 2 h showed ambient temperature-dependent changes in rectal temperature, hypothermia at temperatures below 30 degrees C, and hyperthermia at 35 degrees C and above. Adrenalectomized (Adre) rats showed more hypothermia compared to sham operated controls at 25 +/- 2 degrees C. The increased hypothermia in adrenalectomized rats was reversed by 10 mg/kg IP or 100 microgram/rat ICV of hydrocortisone. Groups of rats pretreated with desmethylimipramine (DMI, 25 mg/kg IP) and 6-hydroxydopamine (6-HD, 100 microgram/rat ICV) or methyl ester of parachlorophenylalanine (ME-PCPA, 100 microgram/rat ICV for 3 days) or 5,6-dihydroxytryptamine (DHT, 75 microgram/rat ICV) showed significantly less hypothermia at the end of 2 h of immobilization. Applying analysis of variance test, the hypothermia in Adre, ME-PCPA and DHT groups, was found to be not significantly different from their respective control groups between 0 and 45 min of immobilization but was significantly different between 45 to 120 min of immobilization. DMI-6-HD group however, showed significant difference between 0--45 min only and not between 45--120 min of immobilization. The results suggest that the early phase of immobilization induced hypothermia between 0--45 min is dopamine and the late phase of hypothermia between 45--120 min is 5-hydroxytryptamine mediated.
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PMID:Immobilization stress in rats: effect on rectal temperature and possible role of brain monoamines in hypothermia. 645 54

The mechanism of ethanol induced hypothermia (EIH) was examined by the use of chemically related compounds which inhibit 5-hydroxytryptamine (5-HT) or norepinephrine (NE) reuptake. Desipramine, a tricyclic antidepressant drug (TCA) and NE reuptake inhibitor partially antagonizes EIH. However, Nisoxetine (NE reuptake inhibitor but not TCA) did not abolish EIH. Chlorimipramine, a TCA compound and 5-HT reuptake inhibitor abolishes EIH. Meanwhile, fluoxetine (5-HT reuptake inhibitor, but not TCA) potentiated ethanol induced hypothermia. It was concluded that the antagonism of EIH is probably related to the antidepressant effect of TCA compounds.
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PMID:Effect of biogenic amines reuptake inhibition on ethanol induced hypothermia. 661 50

1. Either electrical stimulation of midbrain raphe nuclei or administration of 5-hydroxytryptamine (5-HT; serotonin) into the preoptic anterior hypothalamus caused hypothermia in conscious rats at ambient temperatures (Ta) of both 8 degrees C and 22 degrees C. The hypothermia was due to decreased metabolic heat production at Ta = 8 degrees C, while at Ta = 22 degrees C the hypothermia was due to both decreased metabolism and increased heat loss (cutaneous vasodilatation). However, at Ta = 30 degrees C, electrical stimulation of midbrain raphe or intrahypothalamic injection of 5-HT caused an insignificant change in the thermoregulatory responses. There was no changes in respiratory evaporative heat loss in response to these treatments at various Ta's. 2. Direct administration of the serotonergic receptor antagonists such as cyproheptadine and methysergide into the preoptic anterior hypothalamus caused hyperthermia in conscious rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. The hyperthermia was due to increased metabolism and cutaneous vasoconstriction. 3. The hypothermia induced by intrahypothalamic administration of 5-HT was antagonized by pretreatment with an intrahypothalamic dose of either cyproheptadine or methysergide in rats at Ta = 22 degrees C. 4. Inhibition of 5-HT neuronal activity with administration of 5-HT into the midbrain raphe regions also caused hyperthermia, increased metabolism and cutaneous vasoconstriction in rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. 5. These observations tend to suggest that the functional activity of serotonergic receptors in the preoptic anterior hypothalamus mediates thermoregulatory responses in the rat. Activation of serotonergic receptors in the hypothalamus decreases heat production and/or increases heat loss, while inhibition of serotonergic receptors in the hypothalamus increases heat production and/or decreases heat loss in the rat.
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PMID:Serotonergic mechanisms in the hypothalamus mediate thermoregulatory responses in rats. 686 35


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