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

Alcohol is a dominant cause of death in urban hypothermia. Drinking alcohol gives a pleasant feeling of warmth. However, experimental studies on humans during relatively short exposure to moderate cold have given inconsistent results concerning heat balance. Longer exposure to colder environmental situations has, particularly with addition of strenous exercise, revealed enhanced heat loss. A warning must be given to drink alcohol beverages in connection with outdoor activities in a cold environment. It gives a feeling of bravery and influences judgement leading to ignoration of prophylactic measures. Alcohol delays the onset of shivering and reduces its duration. It augments cold diuresis thereby diminishing blood volume and physical working capacity. On the other hand, alcohol seems to protect the heart against ventricular fibrillation at low core temperatures. Furthermore ethanol also seems to have some positive properties in freezing cold injuries.
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PMID:Alcohol and cold. 181 78

The circadian variation of decapitation-induced gasping was investigated by measuring the gasping duration of isolated mouse head after decapitation under both normal and restricted feeding conditions. In the normally fed mice, there was a circadian periodicity in the gasping duration: it was longer during the light period than during the dark period. The circadian periodicity was completely reversed by the restriction of food. The circadian periodicity of the gasping duration were conversely parallel to those of body temperature in both normal and feeding restricted mice, and regression analysis revealed a negative correlation between the gasping duration and body temperature. Furthermore, pentobarbital and ethanol, agents that caused hypothermia, markedly prolonged the gasping duration. These findings suggest that there is a circadian periodicity in the brain reactivity after complete ischemia, which may be associated with the changes of body temperature.
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PMID:Circadian periodicity in the duration of decapitation-induced gasping in mice. 181 61

The effect of combined treatment with doxepin and ethanol was tested in mice, rats and rabbits. Doxepin was given in a single dose (5 or 10 mg/kg) or chronically (10 mg/kg/d for 21 days). Doxepin did not affect ethanol toxicity and ethanol-induced impairment of rota-rod performance, but potentiated ethanol-induced hypothermia (only acutely) and prolonged ethanol-induced sleep in mice. Given acutely it potentiated the inhibitory effect of ethanol on locomotor activity in mice, while given chronically it counteracted the ethanol-induced sedation. Doxepin did not interfere with ethanol-induced EEG effects in rabbits, and prevented the development of tolerance to hypothermic, but not to hypnotic effects of ethanol in rats. In general, the interference of doxepin with ethanol was more pronounced after single doses of the drug than after chronic treatment.
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PMID:The effect of doxepin on the central action of ethanol. 182 Oct 42

To test whether N-methyl-D-aspartate (NMDA) receptors have a role in the development of ethanol tolerance, (+)MK-801, an NMDA antagonist, and (-)MK-801, an inactive isomer, were tested in a rapid tolerance paradigm. Results showed that (+)MK-801 blocked the development of rapid tolerance to ethanol in the tilt-plane and hypothermia tests, while (-)MK-801 was ineffective. Neither drug changed the blood ethanol levels in the treated and untreated animals. These data suggest that the known role of NMDA receptors in long-term synaptic facilitation may underlie the effect of learning in the development of tolerance to the motor-impairing and hypothermic effects of ethanol.
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PMID:NMDA antagonist inhibits rapid tolerance to ethanol. 183 Oct 64

The effect of aminotriazole (AT), inhibitor of catalase activity, on hypothermia and narcosis induced by ethanol and on the acquisition of tolerance to the ethanol hypothermic and narcotic effect was studied. Rats were pretreated with AT (1 g/kg IP) 1 hour before the test dose of ethanol (2.76 g/kg IP) and narcosis time, hypothermia and ethanol blood levels evaluated (first test). For studies on tolerance to ethanol, rats of the first test received daily (for 7 days) a dose of AT (1 g/kg IP) 1 hour before ethanol (2.76 g/kg) given by gavage, and the same parameters evaluated (8th day test). Results were compared to similar groups of rats without AT pretreatment (controls, 1st and 8th day test). Rats pretreated with AT exhibited a shorter narcosis time induced by ethanol but this treatment did not alter the hypothermic effect of ethanol nor ethanol disposal rate. Chronic ethanol treatment induced tolerance to the narcotic and hypothermic effect of ethanol as well as a metabolic tolerance. AT administered daily before the dose of ethanol produced a partial blockade of the development of tolerance to the narcotic effect of ethanol, but did not alter the development of hypothermic or metabolic tolerance. The brain catalase system seems to play a role in narcosis and on the development of tolerance to this effect of ethanol, but not in the hypothermic effect or in the development of tolerance to this ethanol effect. Since the inhibition of liver catalase activity by AT treatment was not correlated with changes in ethanol disposal rate, the liver catalase system appears not to play a role in the metabolic tolerance.
Alcohol
PMID:Effect of 3-amino-1,2,4-triazole on the hypothermic effect of ethanol and on ethanol tolerance development. 187 89

Separately, ethanol and high ambient pressure cause hypothermia in laboratory animals. However, ethanol and high pressure have mutually antagonistic effects on several biological functions and the present experiments investigate their combined action on body temperature. Rats given saline, 1.5 g/kg ethanol or 3.5 g/kg ethanol were exposed to 1 bar air at 25-26 degrees C, 1 bar helium-oxygen at 30-31 degrees C, or 48 bar helium-oxygen at 33.5-34.5 degrees C. Ambient, colonic and tail-skin temperatures were monitored for 60 min. There were no significant differences in mean ambient or tail-skin temperatures between groups belonging to the same ambient condition. Colonic temperatures under the 1 bar conditions were 1.5-2 degrees C lower in the 3.5 g/kg ethanol group than in the saline and 1.5 g/kg ethanol groups, while no significant differences were observed between the groups at 48 bar. Comparisons of the colonic temperatures at the end of the observation period, i.e., 60 min after administration of ethanol, demonstrated that their values at 48 bar were significantly lower than at 1 bar after saline, significantly higher after 3.5 g/kg ethanol and identical across conditions in the 1.5 g/kg groups. The results suggest that high ambient pressure may counteract rather than potentiate the hypothermic effect of ethanol.
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PMID:Effects of ethanol on body temperature of rats at high ambient pressure. 192 10

It has been proposed that ethanol can be oxidized in brain via the peroxidatic activity of catalase and that centrally formed acetaldehyde may mediate several of the psychopharmacological actions of ethanol. The present study was designed to investigate the role of brain catalase in the mediation of ethanol-induced narcosis, hypothermia and lethality in rats. Rats were pretreated with the catalase inhibitor 3-amino-1,2,4-triazole (AT) or saline. Five hours later, animals in each pretreatment group received IP injections of ethanol (3 or 4 g/kg). Ethanol-induced narcosis was significantly attenuated in AT-pretreated rats compared to the saline control group. As well, AT pretreatments reduced significantly the lethal effect of these ethanol doses. However, AT-pretreated ethanol-injected animals significantly reduce their body temperature as compared to the saline-ethanol animals. Blood ethanol determinations revealed that AT did interfere with ethanol metabolism. AT inhibits significantly brain catalase activity at all doses used in this study. The results indicate a role for brain catalase in ethanol effects. Furthermore, they suggest that catalase may be involved in the oxidation of ethanol in brain and that centrally formed acetaldehyde may play a role in ethanol-induced narcosis and lethality, but not hypothermia.
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PMID:Effect of 3-amino-1,2,4-triazole on ethanol-induced narcosis, lethality and hypothermia in rats. 192 13

The hyperglycemic and hypothermic responses to acute ethanol exposure (0, 2, 4, 6 g/kg, intraperitoneally) were examined in non-fasted mice selectively bred for sensitivity (COLD line) or insensitivity (HOT line) to ethanol-induced hypothermia. Blood samples and rectal temperatures were obtained immediately before injection and hourly for 4 hr after injection. As expected, COLD mice demonstrated greater and more prolonged reductions in body temperature than HOT mice, especially at the 4 g/kg dose (HOT: -2.58 degrees C, COLD: -5.08 degrees C). Ethanol produced significant dose-dependent elevations in blood glucose levels over the 4-hr sampling period in both lines. The greatest elevations in blood glucose levels were seen at 4 g/kg, with COLD mice (mean = 225.1 mg/dl) showing significantly greater elevations in blood glucose levels compared to HOT mice (mean = 177.0 mg/dl). These results support the hypothesis that the thermic and glycemic effects produced by ethanol are due to related neural processes that share a common genetic component.
Alcohol Clin Exp Res 1991 Aug
PMID:The relationship between ethanol-induced hyperglycemia and hypothermia: evidence of genetic correlation. 192 51

The effect of ethanol and pentobarbital on in vivo tryptophan hydroxylase activity and its relationship to drug-induced alterations of thermoregulation was examined in long-sleep (LS) and short-sleep (SS) mice. Serotonin function was measured in both the presence and absence of ethanol or pentobarbital in six discrete brain regions. Differences in basal levels of serotonin, 5-hydroxyindole acetic acid or in vivo tryptophan hydroxylase (TpH) activity were found only in the hypothalamus and dorsal raphe nuclei (SS slightly higher). Ethanol (4.2 g/kg i.p) caused significant reductions in in vivo TpH activity in the dorsal and pontine-medullary raphe nuclei and hypothalamus (putative thermoregulatory areas) in both LS (50-60% decrease) and SS (15-30% decrease) mice, but it had no effect on TpH activity in the striatum, cortex or hippocampus. The greater degree of ethanol-induced reduction in TpH activity in LS mice was associated with a greater degree of hypothermia (LS, 4.2 degrees C vs SS, 2.0 degrees C). Pentobarbital had equivalent effects in LS and SS mice on TpH activity in central nervous system thermoregulatory areas (decreases of 40-60%) and on body temperature (decreases of 6.8-7.5 degrees C). When the mice were given ethanol at an elevated environmental temperature (34 degrees C) the hypothermia was almost abolished completely, but depressant effects on TpH activity remained, suggesting that ethanol-induced decreases in TpH activity were direct effects and not secondary to hypothermia. Alterations in ethanol or pentobarbital elimination did not appear to account for the observed differences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serotoninergic involvement in ethanol-induced alterations of thermoregulation in long-sleep and short-sleep mice. 194 31

Schumanniophyton problematicum is a plant popular among Nigerian native healers for the treatment of psychotic patients (madness). An extract obtained by ethanol extraction of the roots caused reductions in respiratory rate, body and limb tone, startle response and spontaneous locomotor activity after i.p. injection in mice, and was capable of inhibiting amphetamine-induced hyperactivity and stereotypic behaviour. It also induced passivity, piloerection, hypothermia and prolonged pentobarbital sleeping time. The i.p. LD50 of the extract in mice was 2.37 g/kg. The effects of the extract appear to be due to depression of central and autonomic system.
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PMID:Neuropsychopharmacologic properties of a Schumanniophyton problematicum root extract. 194 77


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