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

5-Hydroxytryptamine injected into posterior and anterior parts of the pigeon hypothalamus evoked a short lasting hyperthermia or hypothermia, respectively. Variable responses obtained within the same brain region suggest the existence of different 5-HT systems, even in rather limited hypothalamic areas.
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PMID:Opposing temperature responses to intrahypothalamic injections of 5-hydroxytryptamine in the pigeon exposed to cold. 42 99

Antidepressant properties of a new indene derivative, YM-08054-1, and its related compounds were compared with those of tricyclic antidepressants and viloxazine. The potencies of YM-08054-1 to inhibit uptake of both 14C-norepinephrine (14C-NE) and 14C-5-hydroxytryptamine (14C-5-HT) by the rat brain synaptosomes were similar to those of amitriptyline and imipramine. Other indene derivatives with an N-alkylated morpholine ring were proved to have less effect on the uptake of either 5-HT or NE than was YM-08054-1. YM-08054-1 was the most potent among all of the tested antidepressants in the inhibition of reserpine-induced facilitation of convulsions as well as in the potentiation of reserpine-induced facilitation of convulsions as well as in the potentiation of 5-hydroxytryptophan (5-HTP)-induced syndromes in mice, though the inhibitory effect of this agent on reserpine-induced hypothermia was weaker than that of either amitriptyline or desipramine, suggesting relatively selective effects of YM-08054-1 upon 5-HT rather than NE uptake in vivo. Neither viloxazine nor iprindole potentiated the responses to 5-HTP. YM-08054-1 was devoid of peripheral anticholinergic activity and exhibited weak local anesthetic effect as well as low acute toxicity when compared with amitriptyline. The results indicate that YM-08054-1 has a novel profile as an antidepressant agent which is quite different from that of either viloxazine or tricyclic compounds.
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PMID:Pharmacological and biochemical studies on a new compound, 2-(7-indeyloxymethyl)morpholine hydrochloride (YM-08054-1), and its derivatives with potential antidepressant properties. 48 6

During the first days of life 10 microgram i.c.v. 5-HT evoked a primary, short-lasting hyperthermia in kittens and hypothermia in guinea-pigs. In both species, a secondary late hyperthermia occurred that could be prevented by indomethacin pretreatment.
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PMID:5-hydroxytryptamine induced changes in body temperature of newborn kittens and guinea-pigs and the effect of indomethacin thereon. 62 Jul 37

Role of brain monoamines in the hyprothermic activity of cannabis resin (CI) in albino rats was studied using agents which influence monoamine synthesis, storage, release, reuptake, metabolism and receptor activity and monoaminergic neuronal activity. Delta-9-tetrahydrocannabinol content of resin was estimated to be 17%. Reserpine was used for comparison. CI was given orally in the dose of 50 mg/kg. Nialamide (NM) and alpha-methyl-metatyrosine (MMT) caused slight hyperthermia. p-Chlorophenylalanine (PCPA), alpha-methol-p-tyrosine (MPT), 5,6-dihydroxytryptamine (DHT, icv) and 6-hydroxydopamine (6-HD, icv) had no effect on body temperature. alpha-Methyl-dopa (m-Dopa), diethyldithiocarbamate (DDC), DDC with l-Dopa, gammabutyrolactone (GBL), phentolamine (PHENT), phenoxybenzamine (PBZ), propranolol (PROP) and imipramine (IMP) produced hypothermia. Hyprothermic activity of CI was potentiated by NM and PCPA, unaffected by DHT and m-Dopa, blocked by MMT, MPT, 6-HD, GBL, PHENT, PROP and chlorpromazine (CPZ), inhibited by DDC, DDC and l-Dopa and PBZ. CI induced hyperthermia in tolerant rats could be reversed to hypothermia by IMP. Reserpine hypothermia was blocked by NM, MPT, 6-HD and CPZ. There was a partial cross tolerance between cannabis and reserpine. Studies indicate that the hypothermic activity of CI similar to that of reserpine is mediated through central catecholamines and not 5-HT, and that noradrenaline is involved and not dopamine. However, the mechanism of action of cannabis and reserpine on noradrenergic neurone seems to be different.
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PMID:Role of catecholamines in the hypothermic activity of cannabis in albino rats. 82 62

Ergometrine (EGM), 40 mg/kg ip or 100 microgram ivc, produces strong and long-lasting increase of locomotor activity of the rat, completely prevented by pretreatment with spiperone, 0.4 mg/kg, ip, or pimozide, 4 mg/kg ip. Given at a dose of 100 microgram ivc EGM produced a deep hypothermia, resistant to spiperone pretreatment (0.4 mg/kg ip). EGM decelerates cerebral serotonin (5-HT) turnover in mice and rats as measured by accumulation of 5-hydroxyindoleacetic acid after pretreatment with probenecid, and depresses the accumulation of 5-HT in the rat brain stem after pretreatment with pargyline. EGM potentiates the hind limb flexor of spinal rat. This effect is blocked by cyproheptadine (1 mg/kg ip) and danitracen (3 mg/kg ip). The results indicate that EGM stimulates both dopamine and 5-HT receptors in the central nervous system.
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PMID:Dopaminergic and serotonergic effects of ergometrine. 88 3

The effects of changes in ambient and central temperature, amines, PGEu and pyrogen were investigated with respect to the mechanism of Na+-Ca++ ratio in the posterior hypothalamus of the unrestrained cat. Guide tubes were implanted bilaterally above the posterior hypothalamic area of 23 cats so as to accommodate push-pull cannulae. After a Na+ or Ca++ sensitive site was identified by perfusion at 50 mul/min of an artificial CSF containing 10.4 mM excess Ca++ ions or 13.6 mM excess Na+ ions, several types of experiments were undertaken with the results summarized as follows: if the cat was exposed to a cold or warm environmental temperature as the posterior hypothalamus was perfused with excess cation, the typical hypothermia was produced by Ca++ and hyperthermia by Na+ ions. However, if the cat was exposed to peripheral cooling or warming 30 min prior to the perfusion, the fall or rise produced by Ca++ or Na+ was attenuated or prevented. In other experiments, 1.0 muCi 45Ca++ was injected in the ion sensitive site in the posterior hypothalamus to label stores of the cation. Raising of ambient temperature caused a retention of 45Ca++ in this hypothalmic area, whereas a cold environmental temperature enhanced the efflux of 45Ca++ at the same perfusion site. The magnitude of change in 45Ca++ efflux depended upon the intensity of the thermal challenge. Similarly, warming of the anterior hypothalmic, preoptic area by means of implanted thermodes caused an immediate diminution in 45Ca++ efflux in the posterior hypothalamus, whereas cooling of this anterior region augmented the extrusion of 45Ca++ ions from the posterior area. When substances which produce a temperature change were applied to the same thermosensitive zone, the direction of shift in 45Ca++ flux in the posterior area corresponded to the signal for heat production or heat loss. That is, the microinjection of 5-HT, PGE1 or Salmonella typhosa into the anterior hypothalamus enhanced the efflux of 45Ca++ in the posterior hypothalamus as hyperthermia developed, whereas a similar microinjection of norepinephrine reduced the 45Ca++ output from the same sites. Finally, locally anesthetizing the cells of the anterior hypothalamus by the nerve blocker, procaine, prevented the cold and heat-induced 45Ca++ eflux and retention, respectively. These results suggest that if the Na+-Ca++ ratio in the posterior hypothalamus establishes and maintains the set-point for body temperature of 37 degrees -38 degrees C, the mechanism of lability of Ca++ through changes in binding characteristics, transport, or metabolism of the cation serves two purposes: (1) the active defense of the set-point temperature through gradations in ion shifts; and (2) the upward or downward change in set-point value, pathological or normal, triggered by virtue of impulses relayed from the anterior hypothalamus.
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PMID:Hypothalamic Na+ and Ca++ ions and temperature set-point: new mechanisms of action of a central or peripheral thermal challenge and intrahypothalamic 5-HT, NE, PGEi and pyrogen. 97 10

Influences of hyper- and hypothyroidism on MAOI (tranylcypromine) were studied by measuring the effects on rectal temperature and 5-HT, 5-HIAA and norepiniphrine levels and tyramine uptake in the brain. Hyperthyroidism was accomplished in rats injected with triiodothyronine 0.2 mg/kg i.p. every two days for 70 days (long period group) or every day for 5 days (short period group) and hypothyroidism induced by feeding rats a diet to which 0.3% propylthiouracil had been added for 70 days (long period group) or 30 days (short period group). Those controls were treated with a triiodothyronine vehicle 1.0 ml/kg i.p. and fed a normal-balanced diet for each period. All the long period groups were decapitated on the last day and the brains were used for the determination of steady levels of above-cited monoamines. The 5-HT content in hypothyroid rats was considerably higher than euthyroid rats but other determinations in both hyper- and hypothyroid rats did not differ significantly in comparison with euthyroid controls. Each short term group was treated with tranylcypromine 10 mg/kg i.p. on the last day. Tranylcypromine brought about a marked hyperthermia in hyperthyroid rats but conversely hypothermia in hypothyroid rats, while "MAOI-induced 5-HT and norepinephrine increase, 5-HIAA decrease and tyramine uptake inhibition in the brain" of hyper- and hypothyroid rats were almost to the same in degree as in euthyroid rats.
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PMID:[Influences of deviations of thyroid functions on the effects of MAOI in rats--changes of 5-HT, 5-HIAA and norepinephrine contents and tyramine uptake by the brain and fluctuation of the rectal temperature]. 98 51

1. The effect of various agents injected into the cerebral ventricles of the mouse, upon the tremor and hypothermia produced by oxotremorine (0.5 mg/kg i.p.) was studied. 2. Acetylcholine (0.1-10 mug) produced a dose-dependent potentiation of oxotremorine tremor in contrast to the multiphasic effect it had on the accompanying hypothermia. Both tremor and hypothermia were antagonised by very small doses (0.1-10 ng) of atropine. 3. Dopamine and apomorphine (0.1-10 mug) had no significant effect on oxotremorine tremor. A dose-dependent potentiation of hypothermia was, however, observed. 4. Noradrenaline (0.1-10 mug), phentolamine and propranolol (0.1-10 mug) produced no significant effect on tremor and inconsistent results were obtained on hypothermia. 5. Neither tremor nor hypothermia were affected by 5-hydroxytryptamine (1-20 mug). 6. Oxotremorine tremor appears to be due solely to the activation of cholinergic pathways, whereas the production of hypothermia is brought about via a system involving both cholinergic and dopaminergic components. 5-Hydroxytryptamine is not involved.
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PMID:Modification of oxotremorine tremor and hypothermia by injections of drugs into the cerebral ventricles of the mouse. 101 35

1 Three salts of 5-hydroxytryptamine, the hydrogen maleinate, the oxalate and the creatinine sulphate were infused into the hypothalamus of 10-18 day old chickens at ambient temperatures in and below the thermoneutral range. Body temperature was recorded and behaviour observed. Electrocortigrams were recorded in experiments in which 5-hydroxytryptamine hydrogen maleinate was used. The effects of a monoamine oxidase inhibitor and methysergide on these responses were similarly studied. 2 At thermoneutrality (31 degrees C) all 3 salts produced behavioural sleep. 5-Hydroxytryptamine oxalate had inconsistent effects on body temperature. 5-Hydroxytryptamine creatinine sulphate produced hypothermia at small doses and mild hyperthermia at higher doses. 5-Hydroxytryptamine hydrogen maleinate produced hypothermia at all doses tested; the falls in temperature induced by this salt were intensified in magnitude and duration by monoamine oxidase inhibition unlike the responses to the other 2 salts. 3 At temperatures below thermoneutrality (16 degrees C) all 3 salts produced behavioural sleep and electrocortical sleep was recorded with 5-hydroxytryptamine hydrogen maleinate. All 3 salts produced hypothermia, which was intensified in magnitude and duration by monoamine oxidase inhibition. 4 The hypothermia produced by 5-hydroxytryptamine hydrogen maleinate was prevented by equimolar doses of methysergide. 5 The position of the cannula in the hypothalamus was found to be crucial. 6 The results contrast with those found in the adult fowl. No conclusion is drawn as to the relationships of the actions of these salts when infused compared with the effects of endogenous 5-hydroxytryptamine release.
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PMID:Some central effects of 5-hydroxytryptamine in young chickens at and below thermoneutrality. 112 91

Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.
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PMID:The effect of beta-phenylethylamine on temperature in mice and its possible mechanisms of action. 124 22


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