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)

DL-alpha-methyl-p-tyrosine methyl ester hydrochloride affected the hyperphagia and hypothermia characteristic of the genetically obese mouse (genotype, ob/ob) throughout an experimental period of 5 days. Intraperitoneal injections of 100 mg/kg body weight, daily, resulted in a significant increase in the average daily food consumption by 60 per cent, already elevated 35 per cent above that of lean litter-mates. The drug, administered at the same dose, caused a similar percentage elevation of food intake in the lean litter-mates. Rectal temperatures of obese mice were raised significantly throughout the 5-day period by an average of 0.95 degrees C, following administration of the drug. There was a significant rise of 0.75 degrees C in the rectal temperature of lean mice on 2 of the 5 days in the period. Body weight remained unchanged. Further experiments are necessary to determine the site of action at which DL-alpha-methyl-p-tyrosine brings about these effects at this dose in lean and obese mice.
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PMID:Potentiation of hyperphagia and relief of hypothermia in the genetically obese mouse (genotype, ob/ob) by alpha-methyl tyrosine. 3 36

A single intraperitoneal (i.p.) injection in mice of apomorphine (I) and its analogues norapomorphine (II), N-ethylnorapomorphine (III), N-n-propylnorapomorphine (IV) and apocodeine (V), caused dose-related decreases in deep-core body temperature. The neuroleptic agent haloperidol blocked the hypothermia produced by these apomorphines but alpha-methyl-p-tyrosine failed to do so. This indicated a direct post-synaptic stimulation of dopamine receptors. Methysergide potentiated the hypothermic effect of the apomorphine analogues. Taking the amount of apomorphine to produce a 3 degree C fall in temperature at 30 min as unity, the approximate relative potencies were: I 1.00, II 0.06, III 47.50, IV 85.00, V 0.340. The doses of the apomorphines needed to produce hypothermia were much less than those needed to cause stereotypy. The ratios of the minimal doses required to produce hypothermia, to those producing stereotypy were: I 8.82, II 4.00, III 125.00, IV 28.50, V 1.43.
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PMID:Hypothermic effects of apomorphine homologues in mice. 3 2

1. A dose-related hyperthermia is obtained in mice with TRH administered intraperitoneally. 2. This hyperthermia is reinforced by amphetamine given at doses which usually cause hypothermia. 3. p-Chloroamphetamine and L-Dopa also reinforce TRH hyperthermia. Apomorphine is not significantly active. 4. TRH hyperthermia is lowered significantly by alpha-methyl-tyrosine and haloperidol but not significantly by pimozide and chlorpromazine. TRH + Amph hyperthermia is not lowered by any of the DA antagonists tested even at doses reversing Amph hyperthermia. Direct participation of DA receptors is then doubtful. 5. All these variations of temperature have their acme a 15 min except for reserpine which, given 22 hours before, potentiates TRH + Amph hyperthermia after 30 min.
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PMID:Is a dopaminergic system involved in thyrotropin releasing hormone induced hyperthermia and in its potentiation by amphetamine? 4 68

Cocaine injected intraperitoneally into rats resulted in a dose-dependent hypothermia. Intracerebral injection of smaller doses also produced a fall in body temperature. In rabbits and guinea-pigs, cocaine produced hyperthermia, in mice and chicks it produced hypothermia while inconsistent changes were produced in goats. Pre-treatment of rats with 6-hydroxydopamine, alpha-methyl-m-tyrosine or haloperidol significantly antagonized the cocaine hypothermia. Pre-treatment of the rats with either hyoscine or methscopolamine resulted in some but non-significant attenuation of the cocaineinduced hypothermia. Pre-treatment with p-chlorophenylalanine, however, did not modify the cocaine hypothermia. Pargyline pre-treatment significantly antagonized the hypothermic action of cocaine. It is suggested that cocaine may cause the release of noradrenaline centrally or it may potentiate its action by interfering with the uptake mechanism. It is also possible that cocaine may have a direct effect on the heat regulating centre in the hypothalamus.
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PMID:Hypothermic effect of cocaine in rats. 13 13

Blood glucose, lactate, plasma free fatty acid and plasma and tissue individual free amino acid levels were followed in newborn rabbits exposed for 10 h to an environmental temperature of 25 degrees C. Severe hypothermia developed with an increase of blood lactate and accumulation of total free amino acids in plasma and liver. Alanine, isoleucine, leucine, valine, phenylalanine, tyrosine, ornithine and taurine were elevated in the plasma; alanine and ornithine in the liver; leucine and isoleucine in the muscle.
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PMID:The metabolic effects of cold exposure in the newborn rabbit. 48 11

Profound hypothermia (6 degrees C) was induced in cold exposed golden hamsters (Mesocricetus auratus) by a combination of drugs that potentiate brain serotonergic activity (fluoxetine and pargyline) and inhibit noradrenergic activity (alpha-methyl-p-tyrosine). Individual drugs and combinations of 2 were ineffective.
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PMID:Profound hypothermia in golden hamsters (Mesocricetus auratus) induced by serotonergic potentiating and noradrenergic inhibiting drugs. 65 38

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

Lisuride hydrogen maleate induced stereotyped behaviour in normal as well as in reserpinized mice. It antagonized the motor depression and hypothermia induced by reserpine. On i.p. administration the compound was about as effective as apomorphine and D-amphetamine. As with apomorphine and in contrast to D-amphetamine the effects of lisuride hydrogen maleate in reserpinized mice were not impaired by additional treatment with alpha-methyl-p-tyrosine methylester. In untreated mice, the substance was very potent in lowering body temperature with significant hypothermia measured after dosages as low as 0.10 mg/kg i.p. Occurrence of stereotyped behaviour and hypothermia could be prevented by the dopaminergic antagonist haloperidol. From these data it is concluded that lisuride hydrogen maleate in addition to its interaction with serotoninergic systems is a potent dopaminergic agonist with a probably direct action on dopaminergic receptors. Further arguments in support of such an action of lisuride hydrogen maleate are, in addition to biochemical data, its serum prolactin lowering effect in rats, its strong emetic action in dogs and its effects on rat behaviour.
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PMID:Direct dopaminergic action of lisuride hydrogen maleate, an ergot derivative, in mice. 94 66

Pretreatment with valine (0.5-2.0 mmoles/kg) can suppress the hypothermic response of rats placed in a 4degreesC environment and given d-amphetamine sulfate (5 or 10 mg/kg). The amino acid was most effective when given 30 minutes before amphetamine administration, at which time it also significantly lowered brain tyrosine concentration (and, presumably, suppressed catecholamine synthesis). Because dopaminergic neurons mediate the hypothermic response to amphetamine and because amphetamine's ability to produce hypothermia requires, in part, the release of newly synthesized dopamine, these observed effects of valine pretreatment support the hypothesis that treatments which alter precursor (tyrosine) availability also affect brain catecholamine synthesis.
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PMID:Suppression of amphetamine-induced hypothermia by the neutral amino acid valine. 99 76

The intraperitoneal administration of sodium salicylate, L-tryptophan, and tyrosine resulted in significant hypothermia when rats were exposed to a 4degree C ambient temperature. Salicylate and tryptophan increased plasma levels of nonprotein-bound tryptophan while total and bound tryptophan were reduced in salicylate-treated rats. Tryptophan concentrations were unaffected by tyrosine administration. Concomitant with increases in free plasma tryptophan, there occurred significant rises in brain levels of tryptophan in both groups of rats, while brain tyrosine levels were increased in those rats receiving tyrosine. Similarly, significant increments in hypothalamic serotonin levels in rats receiving salicylate or L-tryptophan and increases in hypothalamic norepinephrine in tyrosine-treated rats seem to reflect the increased availability of tryptophan and tyrosine for monamine synthesis. However, alternative mechanisms of hypothermiaseem to be operative since oxygen consumption studies demonstrate dissimilar results for tryptophan and salicylate administration.
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PMID:Salicylate, tryptophan, and tyrosine hypothermia. 113 May 45


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