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

1 The cerebral ventricles of dogs under intravenous pentobarbitone sodium anaesthesia, were perfused with artificial cerebro-spinal fluid (CSF) at a rate of 0.4-0.5 ml/min from the ventricular to the aqueductal cannulae. The effluent was collected from the aqueductal cannula in 20 min samples. The animals' temperatures were recorded from the rectum.2 gamma-Aminobutyric acid (GABA) 0.1-5 mg when injected into the ventricles produced variable temperature effects. Doses of 0.1 and 0.5 mg always produced hyperthermia and 1 and 5 mg doses sometimes produced hyperthermia and sometimes hypothermia.3 Intraventricular perfusion with 2-bromolysergic acid diethylamide (BOL) and hyoscine did not block hyperthermia. Tests on the rat isolated stomach strip or the guinea-pig isolated superfused ileum for the possible release, respectively, of 5-hydroxytryptamine or acetylcholine by GABA were negative.4 When tested for the presence of prostaglandin E(PGE)-like substances on the isolated rat stomach strip, both the control effluent and the GABA effluent showed activity, the latter being much more potent. There was a temporal correlation between this effect and hyperthermia. Intraventricularly administered sodium salicylate converted the GABA-induced hyperthermia to hypothermia and blocked the release of PGE-like substances.5 Hypothermia induced by GABA alone or in the presence of sodium salicylate was associated with the release of noradrenaline into the effluent.6 Intraventricular administration of GABA in reserpinized dogs produced hyperthermia and not hypothermia. Similar results were obtained with phentolamine perfusion in normal dogs.7 Perfusion with calcium-free solution blocked both the noradrenaline-releasing and hypothermic actions of GABA.8 It is concluded that hyperthermia associated with intraventricular injections of GABA is due to the release of PGE-like substance and hypothermia is due to the release of noradrenaline.
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PMID:Analysis of the effects on body temperature of intracerebroventricular injection in anaesthetized dogs of gamma-aminobutyric acid. 415 52

1. Intraperitoneal administration of graded doses of tetrahydronaphthylamine (THN) to rats caused a dose dependent decrease in body temperature.2. Intracisternal injection of graded doses of THN induced hypothermia, and implantation of crystalline THN rostral to the medial preoptic area and caudal to the striatum, caused hyperthermia.3. Pretreatment of the rats with a MAO inhibitor changed the hypothermia into hyperthermia.4. Intraperitoneal injection of 5-hydroxytryptophan caused a hypothermia which could be reversed into hyperthermia when the rats were pretreated with a MAO inhibitor.5. Pretreatment with parachlorophenylalanine enhanced the THN-induced hypothermia.6. Depletion of brain monoamines by Ro-4-1284 in combination with an inhibition of the biosynthesis of noradrenaline (diethyldithiocarbamate) changed the THN-induced hypothermia into hyperthermia.7. It is concluded that THN affects body temperature in rats by two central mechanisms, viz. a decrease mediated by noradrenaline, probably in the hypothalamus, and an increase which might be mediated by 5-hydroxytryptamine rostral to the medial preoptic area.
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PMID:Role of noradrenaline and 5-hydroxytryptamine in tetrahydronaphthylamine-induced temperature changes in the rat. 425 29

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

1. Ouabain given by intracerebroventricular injection to mice in small doses (0.1-0.4 mug) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0.4 mug were excitatory, convulsant and lethal.2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine.3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain.4. The depressant effects were associated with a marked elevation of whole-brain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-beta-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible mode of action of intracerebroventricularly injected ouabain.
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PMID:Pharmacological properties of centrally administered ouabain and their modification by other drugs. 432 23

1. An intravenous injection into rats of 1 mg/kg (-)-Delta(9)-tetrahydrocannabinol Delta(9)-THC) had no effect on rectal temperature and produced in the subcellular fractions of the brain a shift of 5-hydroxytryptamine (5-HT) from the particulate or ;bound' 5-HT to the supernatant or ;free' fraction, whereas the noradrenaline (NA) decreased in both fractions.2. Pretreatment of rats by an intravenous injection of 1 mg/kg Delta(9)-THC three times a week for four weeks, prevented the hypothermia and the reduction in brain 5-HT produced by an intraperitoneal injection of 15 mg/kg reserpine given 24 h after the last Delta(9)-THC injection.3. Pretreatment of rats by a single intravenous injection of 1 mg/kg Delta(9)-THC prevented the hypothermia and reduction in brain 5-HT produced by an intraperitoneal injection of reserpine given 1 h before. The reduction in brain NA was not prevented except at the 18 h time interval.4. An injection of 1 mg/kg Delta(9)-THC intravenously into rats 3 h after an intraperitoneal injection of reserpine accentuated the reserpine hypothermia as well as the reduction of 5-HT but not of NA in the brain.5. The reserpine hypothermia was not prevented by a single intravenous injection of 1 mg/kg Delta(9)-THC when cinanserin, a 5-HT inhibitor, was injected 30 min before the reserpine.
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PMID:The effects of (-)-delta9-tetrahydrocannabinol on reserpine-induced hypothermia in rats. 479 31

1. The hypothesis of Roberts & Broadley (1965) that noradnamine formation in the brain is responsible for endogenous depression has been investigated in mice.2. Injections of noradnamine given directly into the lateral ventricles caused convulsions and profound hypothermia, but were without effect if given subcutaneously.3. The hypothermia, but not the convulsions, induced by noradnamine was reversed by imipramine-like antidepressant drugs given before or after the injection of noradnamine. The convulsions but not the hypothermia were abolished by phenobarbitone.4. Increasing doses of nortriptyline produced a parallel shift of the hypothermic log dose-response curve for intraventricular injections of noradnamine to the right.5 The minimal effective dose of nortriptyline required to reverse noradnamine hypothermia was the same whether the nortriptyline was injected directly into the lateral ventricle or subcutaneously.6. No evidence was found to substantiate the claim that reserpine hypothermia is mediated by noradnamine formation in the brain.7. Intraventricular, but not intraperitoneal, injection of noradnamine caused a depletion of brain noradrenaline and an increase in brain 5-hydroxytryptamine. These changes did not result from the convulsive activity and were not modified by pretreatment with nortriptyline. No effect on heart noradrenaline levels was recorded.8. Noradrenaline, given subcutaneously, also antagonized the hypothermic response to noradnamine.9. The reversal of noradnamine hypothermia by both noradrenaline given subcutaneously and nortriptyline was blocked by alpha and beta-adrenoceptive receptor blocking agents.10. It is considered that the mode of action of the antagonism of noradnamine hypothermia by imipramine-like antidepressant drugs is a peripheral and not a central mechanism and probably results from a potentiation of the effects of circulating noradrenaline released by noradnamine.
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PMID:The interactions of noradnamine and imipramine-like antidepressant drugs. 576 31

Administration of pure 1-delta(9)-tetrahydrocannabinol to mice had the following dose-dependent nzeurochemical and behavioral effects: a slight but significant increase in concentrations of 5-hydroxytryptamine in whole brain; a decrease in concentration of norepinephrine in brain after administration of low doses and an increase after high doses; diminished spontaneous activity, mloderate hypothermnia, hypersetisitivity to tactile and auditory stimiuli, and ataxia after low doses; and sedation, pronounced hypothermia, and markedly diminished spon taneous activity and reactivity after high doses. The duration of the effects on body temperature and spontaneous activity correlated generally with the changes in brain amines. The characteristic changes in brain amines do not correspond exactly to those observed with other psychotropic drugs.
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PMID:1-delta9-tetrahydrocannabinol: neurochemical and behavioral effects in the mouse. 577 12

1. Changes in temperature were determined following injection of noradrenaline, adrenaline, isoprenaline, dopamine and 5-hydroxytryptamine (5-HT) into the cerebral ventricles of the conscious mouse.2. Noradrenaline (1-20 mug) and dopamine (10-160 mug) caused falls in body temperature. Adrenaline (1-20 mug) caused a slight and transient rise in body temperature followed by a fall. Isoprenaline (5-20 mug) caused a rise in body temperature, hypothermia only occurring after very high doses (200 mug) of this catecholamine.3. alpha- and beta-adrenergic blocking agents, phentolamine (> 2 mug) and propranolol (> 5 mug) respectively, caused falls in body temperature when injected into the cerebral ventricles of the mouse.4. Specific drug antagonism studies were limited owing to the intrinsic effects of the alpha- and beta-adrenergic blocking agents. However, some evidence was obtained to indicate that noradrenaline mediated its effects through a central alpha-type adrenergic receptor.5. 5-HT (10-160 mug) caused a fall in body temperature. The action of this indoleamine and the catecholamines in regard to thermoregulatory function is discussed.
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PMID:Temperature changes produced by the injection of catecholamines and 5-hydroxytryptamine into the cerebral ventricles of the conscious mouse. 605 3

The N-desmethyl metabolites of imipramine and amitriptyline possess antidepressant activity in their own right. To test whether this is also true of desmethylclomipramine, studies have been carried out on appropriate models. Desmethylclomipramine was shown to be present in plasma in higher concentrations than the parent compound, to be strongly active in reversing or suppressing reserpine-induced hypothermia, to possess anticholinergic activity on gastrointestinal smooth muscle, inhibiting motility and antagonizing muscarinic receptors, though to a lesser extent than clomipramine. It is also a more potent inhibitor of noradrenaline and dopamine uptake than clomipramine is, though less potent in inhibiting 5-hydroxytryptamine uptake. The metabolite has antidepressant activity of its own, probably associated with its monoamine uptake inhibitory properties, and doubtless makes an important contribution to the efficacy of treatment of depression with clomipramine; for this reason plasma levels of the metabolite as well as those of the parent compound should be taken into account.
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PMID:Some pharmacological aspects of desmethylclomipramine. 610 7

Intraperitoneal administration of prostaglandin E1 (PGE1) produced a hypothermia in rats at room temperatue (22 degrees C). The hypothermia in response to PGE1 was due to cutaneous vasodilatation and decreased metabolic heat production. Depletion of brain 5-hydroxytryptamine (with 5,6-dihydroxytryptamine and p-chlorophenylalanine) did not alter the PGE1-induced hypothermia. However, depletion of bran catecholamines (with 6-hydroxydopamine) and blockade of central catecholaminergic receptors (with phentolamine and propranolol) both greatly reduced the PGE1-induced hypothermia. The data indicate that PGE1 lowers body temperature in rats by acting on the central catecholaminergic systems.
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PMID:The catecholamine mechanisms of prostaglandin E1-induced hypothermia in rats. 610 85


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