Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of sodium fluoride (NaF) induced hypothermia was investigated on relations between the monoamine synthesis and metabolism in the rabbit brain. Five male rabbits per a group, weighing about 2.5kg and having rectal temperatures of 38.4 to 39.3 degrees C, were used in this experiment. The rectal temperature measurements were made by means of an electric thermometer for 5 hours at intervals of 15 or 30 minutes. Through this experiment, animals were housed in a room kept at 22 to 23 degrees C. The following drugs were used in this experiment: NaF (40 mg/kg i.v.), barbital sodium (0.1 g/kg s.c.), hexamethonium bromide (C6, 10 mg/kg i.v.), ergotamine tartrate (30 mg/kg s.c.), phenoxybenzamine hydrochloride (15 mg/kg i.v.), propranolol hydrochloride (5 mg/kg s.c.), pindolol (0.3 mg/kg s.c.), atropine sulfate (30 mg/kg s.c.), 2, 4-dinitrophenol (DNP, 20 mg/kg i.v.), l-DOPA (20 mg/kg i.v.), 5-HTP (20 mg/kg i.v.) Results 1. Intravenous injection of 30 mg/kg of NaF induced a drop of 0.66 degrees C in rectal temperature. 2. Pretreatment with 0.1 mg/kg of barbital sodium or 10 mg/kg of C6 prominently inhibited the NaF-induced hypothermia. 3. The alpha-blockade caused by ergotamine tartrate and phenoxybenzamine or the beta blockade by propranolol hydrochloride and pindolol resulted in an approximate 50% inhibition of maximum drop in body temperature induced by NaF administration. Both alpha- and beta-blockades caused by ergotamine tartrate and propranolol or by phenoxybenzamine and pindolol, however, made a remarkable inhibition of the NaF effect. Cholinergic blockade brought on by atropine sulfate, on the other hand, had no effect against NaF-induced hypothermia. 4. Bilateral splanchnicotomy completely inhibited drops in rectal temperature. 5. Intravenous injection of NaF 40 mg/kg failed to counteract the rise of rectal temperature caused by DNP 20 mg/kg. 6. Pretreatment with l-DOPA made a prominent inhibition of NaF-induced hypothermia. The inhibiting effects of 5-HTP, however, were slight. 7. Administration of NaF made a significant decrease in norepinephrine levels in the rabbit hypothalamus, but had no effect on 5-HT levels.
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PMID:[The rabbit thermo-regulatory system. Effects of high dose of sodium fluoride]. 262 92

A potential antidepressant activity of B-193 was studied in mice and rats. In in vitro studies B-193 did not affect the uptake of NA and 5-HT. In in vivo models the tested compound did not influence the reserpine-induced hypothermia, hypoactivity and ptosis, the stimulating action of L-DOPA, the apomorphine-induced hypothermia. On the other hand, it produced a positive effect in the despair test. When given repeatedly, it evoked adaptive changes in brain neurotransmitter receptors, i.e. it decreased the density of beta-adrenoceptors and increased the number of alpha 1 ones; those changes were accompanied with functional alternations in the reactivity of those receptors: an attenuated behavioral reaction to salbutamol and enhanced aggressiveness induced by a high dose of clonidine. Furthermore, B-193 administered repeatedly enhanced hyperlocomotion induced by amphetamine but did not influence the stereotypy induced by apomorphine. These results indicate that B-193 possesses properties characteristic for atypical antidepressants.
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PMID:Antidepressant profile of 9-methyl-2[-3-(4-phenyl-1-piperazinylpropyl)]-1,2,3,4-tetrahydro-beta- carbolin-1-one (B-193). 263 91

The rectal temperature and serum corticosterone increased in mice exposed to 45 degrees C for 15 min; at the same time, the contents of brain 5-HT and NE reduced, brain DA unchanged. Ginseng root saponins (GRS) ip 200 mg/kg inhibited the increase of serum corticosterone and the decrease of brain 5-HT and NE in heat-stressed mice, but did not affect brain DA. GRS lowered mice body temperature at room temperature and inhibited the rise of body temperature under heat environmental conditions in mice. Reserpine eliminated the hypothermia of GRS at room temperature and its inhibitory effect on hyperthermia under heat-stress conditions. PCPA eliminated only the inhibition of GRS on hyperthermia under heat-stress, but had no significant effect on hypothermia at room temperature.
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PMID:Effects of ginseng root saponins on brain monoamines and serum corticosterone in heat-stressed mice. 264 45

Changes in catecholamines (CA) in the plasma and urine and metabolites of CA and serotonin (5-HT) in the cerebrospinal fluid of guinea-pigs in hypothermia (Trec 30 degrees C) and after subsequent rewarming were determined with HPLC in order to obtain data on early stress reactions and their timing. Both noradrenaline (NA) and adrenaline (A) were low in the plasma but high in the urine after the hypothermic period. These had normalized in the plasma after rewarming but were still high in the urine. Dopamine values tended to be low (not significant). Methoxyhydroxyphenylglycol and homovanilic acid were elevated in the cerebrospinal fluid both after hypothermia and following rewarming, and 5-hydroxyindoleacetic acid after rewarming. The ratio of adrenaline to noradrenaline, the catecholamine hypothermia index, in the urine had risen 24-fold after hypothermia and 40-fold after rewarming. The results support the view that elevated catecholamine concentrations in the urine and elevated values of their metabolites in the cerebrospinal fluid could be regarded as hypothermia markers. However, other stress conditions, which have lasted at least a few hours, should be excluded in the final interpretation.
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PMID:Plasma and urine catecholamines and cerebrospinal fluid amine metabolites as hypothermia markers in guinea-pigs. 274 75

1) The functional effects of the 5-HT1A receptor selective ligand, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) can be divided into effects mediated by presynaptic (somato-dendritic) autoreceptors and postsynaptic receptors. Hypothermic responses in the mice and rat reflect presynaptic effects. Stereotypic motor responses in the rat reflect postsynaptic function. 2) These functional models of 5-HT1A receptor activity have been used to examine the effects of different antidepressant treatments and lithium during acute (24h) and chronic (14 day) administration. 3) Presynaptic 5-HT1A-mediated hypothermia is attenuated by chronic treatment with amitriptyline, desipramine, zimeldine, high dose mianserin, tranylcypromine, lithium and repeated electroconvulsive shock (ECS). Thus, all these treatments may increase tolerance to increased release of 5-HT. 4) Postsynaptic 5-HT1A-mediated motor effects are attenuated by desipramine, zimeldine and ECS but enhanced by lithium. 5) The 5-HT1A receptor appears to be an important locus for the actions of antidepressant treatments and lithium.
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PMID:The effects of antidepressant treatments and lithium upon 5-HT1A receptor function. 274 72

Intraventricular administration of amphetamine in mice produced hypothermia. Pretreatment with the dopaminergic (DA) receptor antagonist haloperidol reduced this response, whereas pretreatment with pimozide, sulpiride or cis-flupentixol did not. The direct DA agonist apomorphine strongly potentiated the hypothermia. Pretreatment with the serotonergic (5-HT) receptor blocker cyproheptadine also potentiated the hypothermia. Depletion of 5-HT in brain by p-chlorophenylalanine and accumulation of 5-HT induced by fluoxetine had no effect. In contrast, stimulation of 5-HT receptors by quipazine reduced the hypothermic effect of amphetamine. The inhibitor of catecholamine synthesis alpha-methyl-p-tyrosine, the alpha-adrenergic blocker phentolamine and the muscarinic antagonist atropine failed to alter the hypothermia. It was concluded that DA and 5-HT mechanisms are involved in amphetamine-induced hypothermia in mice and that these two systems display a functional antagonism.
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PMID:Differential effects of neuroleptic and serotonergic drugs on amphetamine-induced hypothermia in mice. 285 40

The newly synthesized compound and putative 5-HT2 antagonist ritanserin, but not the structurally related compound R 56413, resembles pirenperone in that it acts as a pure antagonist in an LSD-saline drug discrimination assay in the rat. Ritanserin exceeded pirenperone in terms of behavioral specificity; the lowest effective dose of ritanserin in antagonizing LSD was one order of magnitude higher than that of pirenperone, but the compound depressed rate of operant responding only at doses that were about 1000-fold higher than those at which pirenperone was effective. Ritanserin exerted effects in an open field test which were reminiscent of anxiolytic drug activity in the rat; its effects were greater than those of pirenperone, R 56413 and the benzodiazepines chlordiazepoxide and diazepam. The results of experiments on antagonism of 5-HT-induced hypothermia and of the 5-HTP-induced head-twitch response fail to support the possibility that the putative anxiolytic effects of ritanserin in the rat can be ascribed simply to a pharmacologically defined action at 5-HT receptors.
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PMID:Behavioral and 5-HT antagonist effects of ritanserin: a pure and selective antagonist of LSD discrimination in rat. 286 59

The effect of i.p. injection of sodium barbitone and chlorpromazine (25 mg/100 g body wt) on the levels of NE, 5-HT and body temperature was investigated in the brain regions of the field rat and the guinea-pig. Injection of the field rat with barbitone sodium or chlorpromazine provoked a general increase in the NE and 5-HT concentrations of the various brain parts. In guinea-pig variable changes were observed. Following injection with either of the two drugs, hypothermia was induced in the two animals at all of the time intervals examined.
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PMID:Studies of contents of norepinephrine and 5-hydroxytryptamine in brain--II. Effect of sodium barbitone and chlorpromazine. 286 56

In the mouse, injection (subcutaneously) of the putative 5-HT1 agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), produced a dose-related hypothermia (ED50:0.36 mg/kg). A maximum response was elicited by intracerebroventricular (i.c.v.) injection of 8-OH-DPAT (3 micrograms) and almost abolished by lesion of 5-HT-containing terminals in the brain with 5,7-dihydroxytryptamine (5,7-DHT; i.c.v.) or long-term treatment with p-chlorophenylalanine. The response was unaltered by a range of neurotransmitter antagonists: prazosin (alpha1-adrenoceptor), idazoxan (alpha2-adrenoceptor), metoprolol (beta1-adrenoceptor), erythro-DL-1-(7-methylindan-4-yloxy)-3-isopropylamino-but an-2-ol (beta2-adrenoceptor), (-)propranolol or (+/-)pindolol (beta-adrenoceptor), flupenthixol (dopamine) or Ro 15-1788 (benzodiazepine binding site). Classical 5-HT antagonists (methysergide, metergoline, cinanserin and methiothepin) were either without effect or facilitated the response and the 5-HT2 antagonist, ritanserin was also without effect. In contrast, quipazine and haloperidol produced a dose-related antagonism of the response. Since the response was almost abolished by a lesion induced by 5,7-DHT and was antagonised by quipazine, which is known to antagonise presynaptic 5-HT function in vitro, it is suggested that the hypothermic response is due to 8-OH-DPAT acting as an agonist at a presynaptic 5-HT receptor, which also appears to be sensitive to butyrophenones (the antagonism elicited by haloperidol but not by flupenthixol). The hypothermic response of mice to 8-OH-DPAT, therefore, may provide a simple and convenient in vivo model in which to measure the function of the presynaptic 5-HT receptor.
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PMID:The pharmacology of the hypothermic response in mice to 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). A model of presynaptic 5-HT1 function. 286 35

Antagonism of reserpine-induced hypothermia is an animal model used in the screening of antidepressants. The activity of imipramine on this test is partly impaired by propranolol. This effect of imipramine was analyzed using specific adrenoceptor and 5-HT receptor blocking drugs in order to determine the nature of this effect of propranolol. The non-selective beta 1-beta 2 adrenoceptor antagonist, propranolol as the specific beta 1 adrenoceptor antagonist betaxolol, but not the specific beta 2 blocking drug DL-erythro-3-isopropylamino-1-(7-methyl-4-indanyloxy)-2-butanol hydrochloride 313.9 (ICI 118,551), partly antagonized the effect of imipramine at 30 min. None of the serotonin (5-HT) receptor antagonists, methysergide, metergoline, ritanserin and buspirone, impaired the effect of imipramine. On the contrary, methysergide alone antagonized reserpine-induced hypothermia and methysergide or metergoline increased the action of imipramine. Propranolol impaired neither the hypothermia induced by an agonist at the 5-HT 1A receptors: 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) nor the increase in spontaneous motor activity induced by an agonist at the 5-HT 1B receptors: 5-methoxy-3(1,2,3,6-tetrahydropyridin-4-yl)1-H indole (Ru 24,969). It is concluded that the effect of propranolol is not the result of a blockade of 5-HT 1A, 5-HT 1B or 5-HT 2, but is in part due to blockade of beta 1 adrenoceptors.
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PMID:Analysis of the nature of antagonism of the reserpine-induced hypothermia by imipramine. 289 Oct 45


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