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)

A female newborn infant with Marfan-like habitus experienced lethargy and hypothermia associated with tyrosinemia that was not corrected by the administration of ascorbic acid at 50 mg/day but that subsequently responded to ascorbic acid at 500 mg/day. Cerebrospinal fluid analysis for neurotransmitter metabolites showed elevated concentrations of homovanillic acid and 5-hydroxyindoleacetic acid when the child was symptomatic and normal concentrations after successful ascrobic acid therapy. These observations suggest that a high level of tyrosine in serum can affect the metabolism in the brain of dopamine and serotonin.
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PMID:CSF neurotransmitter studies. An infant with ascorbic acid-responsive tyrosinemia. 615 67

It has been suggested that hypothermia induced in rabbits by As2O3 3 mg/kg (i.v.) depends mostly on the blocking of the thermo-regulatory center. The relationship between hypothermia induced by As2O3 and brain monoamine levels in rabbits was investigated. To clarify the mechanism of the hypothermia, the influence of pretreatment with several agents on As2O3-induced hypothermia and on monoamine levels in the hypothalamus was examined. The core temperature was measured by inserting the thermister probe into the rectum and noradrenaline(NA), 5-hydroxytryptamine(5-HT) and 5-hydroxyindoleacetic acid(5-HIAA) levels in the hypothalamus were estimated fluorometrically. Pretreatment with p-chlorophenylalanine(PCPA), alpha-methyl-p-tyrosine(alpha-MPT) or 5-hydroxytryptophan(5-HTP) did not inhibit the hypothermia induced by As2O3 but did decrease NA levels in the hypothalamus. On the contrary, pretreatment with barbital sodium, pheniprazine, 1-DOPA and 1-tyrosine significantly inhibited the hypothermia or exhibited the hyperthermia. As2O3-induced hypothermia in rabbits was followed by a decrease in NA levels and an increase in 5-HT levels in the hypothalamus. On the other hand, when the hypothermia induced by As2O3 was inhibited by pretreatment with barbital sodium, pheniprazine, 1-DOPA and 1-tyrosine, both NA and 5-HT levels in the hypothalamus were significantly increased. These results suggest that As2O3-induced hypothermia is due to a decrease in NA levels and inhibition of the hypothermia is due to an increase in NA levels, in the rabbit hypothalamus.
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PMID:[Studies on As2O3-induced rabbit hypothermia and brain monoamines (author's transl)]. 615 19

Intracerebroventricular (ICV) administration of kyotorphin (L-Tyr-L-Arg) and cyclo (N-methyl-L-Tyr-L-Arg), its analog, produced significant dose-dependent hypothermic responses in mice at an ambient temperature of 24 degrees C. The hypothermic action of kyotorphin was much greater than that of Met-enkephalin (Met-ENK) but less than that of cyclo NMTA. This action was slightly but not significantly reversed by intraperitoneally administered naloxone (8 mg/kg), an opioid receptor antagonist. Met-ENK utilized as a control peptide in this study also produced a dose-dependent hypothermia which was slightly antagonized by naloxone (8 mg/kg, IP). Thyrotropin releasing hormone (TRH) injected ICV produced hyperthermia dose-dependently. The hypothermia induced by kyotorphin, its cyclic analog and Met-ENK was prevented by a small dose of TRH (0.18 microgram = 0.5 nmol/animal) which by itself had little effect on body temperature. A TRH neuronal system in the brain may explain the mechanism of kyotorphin-induced hypothermia. However, there was little evidence of involvement of opioid receptors. The present study demonstrates a potent action of kyotorphin and its analog on thermoregulation.
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PMID:Actions of intracerebroventricular administration of kyotorphin and an analog on thermoregulation in the mouse. 642 2

Relationships between structure and duration of neurotensin's central action were examined. Included in the study were analogs containing amino acid substitutions at purported enzymatic cleavage sites of neurotensin: the arg8-arg9, the Pro10-Tyr11, and the Tyr11-Ile12 peptide bonds. Peptides were administered in rats via the cerebro-ventricular route and the ensuing hypothermia was monitored repeatedly until the effect dissipated. Results indicate that substitutions of the Tyr11 residue of the neurotensin molecule with either Dopa, Trp, D-Trp, or D-Tyr yielded analogs displaying markedly increased durations of action. Substitutions at other sites did not alter the time course of neurotensin's hypothermic effect. The longest acting analog was [Dopa11]-NT. At a dose of 7.5 micrograms the hypothermia induced by this analog persisted for 660 min while the effect of a same dose of neurotensin endured for only 90 min after injection. No clear correlation was found between the relative potency of analogs and their duration of action. Taken together, the results confirm the predominant role of Tyr11 in the inactivation of neurotensin by the brain, but do not support the hypothesis that relative potencies of structural analogs are solely dependent on differing susceptibilities to enzymatic degradation.
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PMID:Relationships between structure and duration of neurotensin's central action: emergence of long acting analogs. 651 48

The role of ethanol-induced hypothermia on some selected biochemical and behavioral parameters was evaluated. Rats were kept from 1 h before to 1 h after injection (saline or ethanol 2 g/kg, 20% solution IP) in an environment chamber at either 22 degrees C or 35 degrees C, and then tested behaviorally or sacrificed. Exposure of rats to a warm environment (35 degrees C) prevented the ethanol-induced hypothermia found in rats kept at 22 degrees C. Ethanol-treated rats kept at 35 degrees C had an attenuated increase in levels of free fatty acids and of corticosterone in plasma, suggesting that part of the ethanol-induced response may result from hypothermia rather than from ethanol itself. In addition, tyrosine levels were unexpectedly increased by 18% in intoxicated animals kept at 35 degrees C. By contrast, gross motor activity tested 1 h after injection was depressed more in animals kept at 35 degrees C than in those kept at 22 degrees C, and swim performance was impaired more at 5-20 min after treatment in animals not showing hypothermia. The greater behavioral impairment was not due to any debilitating effects of the warm environment since the saline control animals showed comparable activity to that of rats kept at 22 degrees C. We conclude that ethanol-induced hypothermia may influence and interact with other actions of ethanol.
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PMID:Biochemical and behavioral effects of acute ethanol in rats at different environmental temperatures. 678 13

The C-terminal octapeptide of cholecystokinin (CCK-8) injected into the lateral ventricle of rats produced a lowering of body temperature. CCK-8 potentiated pentobarbital-induced hypothermia, but not the ethanol one. Thyrotropin releasing hormone (TRH) and prostaglandin E2 (PGE2) antagonized the hypothermic effect of CCK-8. Non-sulfated CCK-8 was ineffective in lowering body temperature, indicating that sulfated tyrosine in the CCK molecule is indispensable for its hypothermic action. Caerulein was found to possess rather less activity compared with CCK-8.
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PMID:Effect of cholecystokinin octapeptide on body temperature in the rat. 680 79

The genetically obese (ob/ob) mouse exhibits defective thermoregulatory responses to cold exposure. Pathophysiological explanations for this phenomenon have focused on abnormalities in intracellular metabolism or insensitivity of peripheral tissues to the thermogenic effects of catecholamines. Because the sympathetic nervous system (SNS) is subject to feedback regulation, a peripheral impairment in thermogenesis should be associated with a compensatory increase in SNS activity. To examine SNS activity in the ob/ob mouse, norepinephrine (NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of ob/ob and lean mice. The results from studies utilizing radiolabeled NE or inhibition of NE biosynthesis with alpha-methyl-p-tyrosine to measure NE turnover demonstrated reductions in SNS activity of 33-56% in heart and of 45-73% in IBAT in ob/ob mice at ambient temperature (22 degrees C) compared with measurements in lean controls. During cold exposure (4 degrees C) NE turnover increased in heart and IBAT to a similar extent in both ob/ob and lean mice, but NE turnover rates in heart, and probably in IBAT as well, remained lower in the obese mice than in the lean despite the gradual development of hypothermia in the ob/ob mice during this period. Administration of naltrexone, a long-acting opiate antagonist, failed to reverse the suppression of SNS activity observed in the ob/ob mice. These data indicate that diminished SNS activity in ob/ob mice may be an additional factor contributing to the defective thermogenesis characteristic of these animals.
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PMID:Diminished sympathetic nervous system activity in genetically obese (ob/ob) mouse. 688 29

Injections of p-chloramphetamine (PCA, 5 mg/kg) induced hypothermia, ejaculation, salivation and irritability in male rats kept at an ambient temperature of 20 +/- 1 degree C. PCA-induced hypothermia was attenuated by pretreatment with the 5-hydroxytryptamine (5-HT) uptake blockers Lundbeck 10-171 (Lu 10-171, 10 mg/kg) and chlorimipramine (CMI, 20 mg/kg) and the 5-HT synthesis inhibitor parachlorophenylalanine (PCPA, 150 mg/kg daily for 3 days); it was potentiated by pretreatment with the noradrenaline uptake blocker Lundbeck 5-003 (Lu 5-003, 10 mg/kg) and the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine (AMPT, 50 mg/kg every 3 hr for 9 hr). PCA- induced ejaculation was attenuated by pretreatment with Lu 10-171 and CMI. PCA-induced salivation was attenuated by pretreatment with Lu 10-171 and CMI and potentiated by pretreatment with Lu 5-003. PCA-induced irritability was potentiated by pretreatment with PCPA. These results suggest that both 5-HT and the catecholamines play a role in PCA-induced hypothermia, ejaculation, and salivation.
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PMID:Mechanisms of PCA-induced hypothermia, ejaculation, salivation and irritability in rats. 719 65

Intravenous injections of different doses of tyramine induced hypothermia in the pigeon in the cold and a moderate hyperthermia in the warm environment. The hypothermia was correlated with a dose-dependent decline in shivering. Hyperthermia was attributed to the chrono- and inotropic effects of tyramine. The indirect stimulatory effects of noradrenaline (NA) at the tissue level were studied. Pretreatment with alpha-methyl-para-tyrosine (alpha-MpT) and blocking alpha-adrenoceptors with phentolamine, diminished the hypothermia induced by tyramine in the cold. The results obtained indicate that the release of endogenous NA stimulated by tyramine might result either in hypothermia or hyperthermia, thus resembling similar effects obtained with exogenous NA in birds.
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PMID:Thermoregulatory responses to tyramine in the pigeon. 721 1

To examine the role of neurotensin in opioid-induced thermo-regulation, Tyr-Pro-N-MePhe-D-Pro-NH2 (PL-017, 1.86 nmol i.c.v.), neurotensin (NT, 0.0747-2.98 nmol i.c.v.), ([trans-(+/-)-3, 4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzenacetamide+ ++]) (U50,488H; U50, 10-40 mg/kg s.c.), dynorphin A1-17 (DY, 4.65 nmol i.c.v.) and DPDPE (4.65 nmol i.c.v.) were injected alone or in combination with NT into unrestrained, male S-D rats. At 20 +/- 2 degrees C ambient, body temperature (Tb) was measured for 3 hr after injection. PL-017 induced dose-dependent hyperthermia; NT, DY and U50 produced dose-related hypothermia. NT (0.0747 nmol) had no effect on PL-017-induced hyperthermia; higher doses of PL-017/NT antagonized the hyperthermia and increased the peak and duration of the hypothermia. Pretreatment with cyclic D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP; 0.74 nmol i.c.v.) blocked the enhanced PL-017/NT-induced hypothermia but had no effect on NT-induced hypothermia. DY/NT reduced Tb dose dependently but the effect did not differ significantly from NT alone. U50 (20 or 40 mg/kg)/NT increased the peak and duration of the hypothermic response. Naloxone pretreatment (10 mg/kg s.c.) blocked the effect of U50 alone and in combination with NT, as did the peripheral opioid antagonist, naloxone methiodide (100 mg/kg s.c.). Nor-binaltorphimine (25 nmol i.c.v.) partially blocked the effect of U50 on Tb and had no effect on NT or U50/NT. DPDPE did not alter Tb alone or in combination with NT. The data presented provide information on the role of NT in opioid-induced thermoregulation.
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PMID:Interaction between opioid agonists and neurotensin on thermoregulation in the rat. I. Body temperature. 761 10


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