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

The antidepressant characteristics of three indole alkylamines were investigated and compared with phenelzine and imipramine by utilising specific pharmacological tools like reserpine, amphetamine, tryptamine and tetrabenazine for determining their possible mechanism of action. Amongst the three indole compounds investigated, indole-3-(2-aminopropyl)-acetate (U-14 164E), indole-3(2-aminobutyl)-d-acetate (u-17 312E) and beta-phenethylhydrazine (phenelzine) produced complete antagonism to reserpine induced sedation, hypothermia as well as facilitation of convulsive seizures. Some of these features suggest that MAO inhibition might be a common mechanism of action of these indoles. The potentiation of CNS effects of tryptamine by these compounds is an outstanding feature of MAO inhibitors, while imipramine is ineffective. Qualitative differences between these indoles and imipramine are evident in the tetrabenazine test. The potentiation of amphetamine induced motor excitation and pentobarbitone narcosis has been explained.
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PMID:A study of antidepressant activity of some indole alkylamines. 2 69

Common effects of four beta-adrenergic blocking drugs have been investigated in mice using classical and new psychopharmacological tests. Propranolol, alprenolol, practolol and penbutolol reduced the increase in locomotor activity produced by reserpine after MAO inhibition; they produce hypothermia when associated with amphetamine and they increase oxotremorine-induced hypothermia. Regarding these three tests the studied substances ranged themseleves in the same order of potency: penbutolol greater than propranolol greater than alprenolol greater than practolol. Propranolol and penbutolol decreased the toxicity provoked in crowded mice by amphetamine or by the association pargyline-reserpine; alprenolol and practolol did not. Propranolol, penbutolol and alprenolol antagonized the amphetamine-induced increase in motor activity; practolol did not. When used at doses for which d-l propranolol was active, the dextrogyre isomer of propranolol was without effect whatever the test studied. It is suggested that for the selection of a beta-blocking drug, regarding central effects in man, the tests described would deserve consideration.
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PMID:[Effects of four beta-blocking agents on some psychopharmacological tests in mice (author's transl)]. 3 71

Various drugs known to bind to serum albumin were examined to determine whether or not they influenced the level of free tryptophan in serum in vitro and in vivo. Possible relationships between the serum free tryptophan level and serotonin (5-HT) synthesis in the brain and the hypothermic effects of these drugs were investigated. Of the drugs examined, sodium salicylate, sodium benzoate and indomethacin caused a significant increase in the concentration of serum free tryptophan and stimulated the synthesis of 5-HT in the brain. Hypothermia induced by salicylate and indomethacin was potentiated by pretreatment with pargyline, a monoamine oxidase inhibitor. Administration of benzoate did not cause any change in body temperature, but after pargyline a hypothermia did occur. However, pretreatment with parachlorophenylalanine, an inhibitor of 5-HT synthesis, did not influence the hypothermia induced by salicylate and indomethacin. Relationship between the hypothermic effect and the increase of 5-HT synthesis in the brain after a large dose of salicylate and indomethacin is discussed.
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PMID:Effects of various drugs on serum free and total tryptophan levels and brain tryptophan metabolism in rats. 12 58

The effects of viloxazine, a clinically effective antidepressant, on noradrenaline (NA) and 5-hydroxytryptamine (5-HT) uptake and various related pharmacological activities were determined and compared to those of the tricyclic antidepressants desimipramine, imipramine, and amitriptyline. Viloxazine inhibitied [3H]NA uptake in the mouse and rat heart, being maximally about one half as potent as imipramine with a similar onset, but shorter duration of action than imipramine. The drug did not inhibit [3H]NA uptake in rat medulla or hypothalamus in contrast to desimipramine and imipramine, but it did alter [3H]NA metabolites in a similar manner. Viloxazine, like desimipramine, was a weak blocker of mouse brain 5-HT uptake, but differed from desimipramine as it poteniated 5-HT-mediated functions in the mouse and rat, as did imipramine and amitriptyline, the latter drugs being relatively potent blockers of 5-HT uptake. Viloxazine potentiated the L-DOPA behavioural syndrome in the mouse, antagonized reserpine-induced ptosis and hypothermia in the mouse, and inhibited gastric acid secretion in the rat, but was less potent than the tricyclic antidepressants. No appreciable in vivo inhibition of monoamine oxidase (EC 1.4.3.4.) activity in the mouse was exhibited. Like imipramine, the drug potentiated the ocular effects of L-adrenaline in the rabbit. It was similar to imipramine in potency in potentiating the apomorphine-induced gnawing in the mouse. The drug antagonized oxotremorine-induced hypothermia in the mouse but differed from the tricyclic antidepressants in not exhibiting the anticholinergic effects of blocking the tremors, salivation and lacrimation. Thus, viloxazine exhibits activities related to the biogenic amines both similar to and different from the tricyclics desimipramine, imipramine, and amitriptyline. These actions appear to be of relevance with respect to the antidepressant action of this drug.
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PMID:Effects of viloxazine, an antidepressant agent, on biogenic amine uptake mechanisms and related activities. 97 78

Mice undergoing withdrawal after chronic ethanol consumption were found to be hypothermic if kept at room temperature. The extent of the hypothermia correlated well with the behavioral withdrawal symptoms and could be used as a quantitative measure of the severity and time course of the withdrawal syndrome. Placing mice in a cold environment (4 degrees C) exacerbated the hypothermia whereas placing animals at 34 degrees C reversed the hypothermia and produced hyperthermia. It was concluded that the temperature set point mechanism and the ability to regulate around this set point was disturbed in animals physically dependent on alcohol. During consumption of the ethanol-containing diets, mice exhibited tolerance to the hypothermic effects of an acutely administered dose od ethanol. Tolerance to the hypothermic effects of ethanol mirrored the development of behavioral tolerance as measured by performance on a tilting plane. Temperature and behavioral tolerance were both shown to extend well beyond the period of the withdrawal syndrome. Ethanol-treated mice were found to be cross-tolerant to the hypothermic effects of barbiturates but not to the hypothermia produced by the monoamine oxidase inhibitor, pargyline.
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PMID:Body temperature in mice: a quantitative measure of alcohol tolerance and physical dependence. 98 76

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

The synthesis and selected pharmacological testing of (+/-)-4-methoxy-beta-hydroxyphenethylamine [1-(4-methoxyphenyl)-2-aminoethanol] and its N-methylated derivatives are presented. Members of this series were found to exert partial prevention of reserpine-induced hypothermia in mice and to inhibit monoamine oxidase in Warburg studies. Activity was essentially dose dependent. The secondary amine was the most active member of the series. The tertiary amine was least active, and the primary amine exhibited intermediate activity.
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PMID:Monoamine oxidase inhibiting activity of a series of (+/-)-4-methoxy-beta-hydroxyphenethylamines. 115 25

5-Hydroxy-5-(4'-chlorophenyl-2, 3-dihydro-5H-imidazo (2, 1-a)isoindole (mazindol), a novel tricyclic compound, has been shown to suppress food consumption in rats at doses causing weak central stimulation and little effects on blood pressure or heart rate. The substance produces dose-related decreases in the consumption of orange juice in cebus monkeys trained on an operant behavior schedule. The compound did not alter cardiac or pulmonary hemodynamics in the anesthetized dog but provided potentiation of norepinephrine pressor responses. Mazindol also demonstrated potent but incomplete antagonism of reserpine-induced hypothermia in mice, antagonism of tetrabenazine catalepsy in rats, and suppression of mouse-killing behavior of rats. Suppression of mouse-killing was reduced by lesions placed in the septal area of the brain. Brain monoamine oxidase or catechol-o-methyl-transferase activities were not altered, although preliminary experiments showed that mazindol reduced uptake of norepinephrine in brain tissue.
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PMID:Pharmacological analysis of a new anorexic substance: 5-hydroxy-5(4'-chlorophenyl)-2, 3-dihydro-5H-imidazo-(2, 1-a) isoindole (Mazindol). 117 62

The administration of TCP (15 mg/kg, i.p.) to rats pretreated with either intraperitoneal RbCl (3 mmol/kg, twice daily for 5 days) or dietary RbCl (30 mmol/kg diet, for 14 days), resulted in the complete 5-HT behavioural syndrome. Pretreatment with p-chlorophenylalanine (i.p. 300 mg/kg x2) or (-)-propranolol (20 mg/kg, i.p.), pindolol (4 mg/kg, i.p.) and ritanserin (0.4 mg/kg, s.c.) prevented the occurrence of the 5-HT syndrome, produced by dietary RbCl plus TCP. Intraperitoneal administration of RbCl had no effect upon the 5-HT behavioural syndrome, produced by 8-OH-DPAT (0.5 mg/kg, s.c.) or 5-MeODMT (2 mg/kg, i.p.) but enhanced the 5-HT syndrome produced by quipazine (20 mg/kg, i.p.), DOI (8 mg/kg, s.c.), p-chloramphetamine (4 mg/kg, i.p.) or by TCP plus L-tryptophan (50 mg/kg, i.p.) in rats. Dietary administration of RbCl resulted in the enhancement of the 5-HT2-mediated head-twitches in the mouse and the attenuation of hypothermia in the mouse, induced by 8-OH-DPAT (0.5 mg/kg, s.c.). The accumulation of 5-HT (after inhibition of monoamine oxidase) and the rate of synthesis of 5-HT in the whole brain (minus cerebellum) were enhanced by dietary and intraperitoneal administration of RbCl, respectively. The effects of lithium and rubidium, respectively, on 5HT function in brain are compared.
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PMID:The effects of rubidium, caesium and quinine on 5-HT-mediated behaviour in rat and mouse--1. Rubidium. 138 43

There have been few studies investigating the effect of treatments that alter serotonergic neurotransmission on the density of serotonin1A (5-hydroxytryptamine1A [5-HT1A]) receptors, even though lesioning serotonergic neurons has been reported to enhance certain responses thought to be due to activation of 5-HT1A receptors and repeated treatment of rats with different types of antidepressants can diminish 5-HT1A-mediated responses. Consequently, the binding of 3H-8-hydroxy-2-(di-n-propylamino)-tetralin (DPAT) to 5-HT1A receptors in serotonergic cell body and terminal field areas of rat brain was measured by quantitative autoradiography following either the lesioning of serotonergic neurons with 5,7-dihydroxytryptamine (5,7-DHT), or after chronic administration of monoamine oxidase inhibitors (MAOIs) (clorgyline, phenelzine, or tranylcypromine) or inhibitors of 5-HT uptake (citalopram or sertraline). Treatment of rats with 5,7-DHT did not cause any significant increase in binding of 3H-DPAT to 5-HT1A receptors in any area of the brain examined. There was no significant reduction in the binding of 3H-DPAT in terminal field areas of serotonergic innervation in rats treated with 5,7-DHT except in the CA2/CA3 region of the hippocampus (33% to 35% reduction). In the dorsal and median raphe nuclei, the specific binding of 3H-DPAT was reduced by treatment of rats with 5,7-DHT. In lesioned rats, the binding of 3H-cyanoimipramine (3H-CN-IMI) to uptake sites for serotonin was essentially eliminated in all terminal field areas examined, as well as in the dorsal and median raphe nuclei. Repeated administration of clorgyline, phenelzine, tranylcypromine, citalopram, or sertraline produced an attenuation of the hypothermic response of rats to acute subcutaneous injection of the 5-HT1A-receptor-agonist DPAT. In spite of this change in 5-HT1A responsivity, these treatments caused in the same animals no consistent change in the binding of 3H-DPAT in either serotonergic cell body or terminal field areas. Of the five drugs studied that diminished DPAT-induced hypothermia, only phenelzine and clorgyline significantly reduced the binding of 3H-DPAT, and even then in only a few of the 12 areas of brain measured. As a result of treatment of rats with tranylcypromine there was a significant increase in the binding of 3H-DPAT in the CA2/CA3 region of the hippocampus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A quantitative autoradiographic study of serotonin1A receptor regulation. Effect of 5,7-dihydroxytryptamine and antidepressant treatments. 202 79


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