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

In acute ethanol studies aminooxyacetic acid (AOAA) alone produced marked hypothermia although a test dose of ethanol was able to produce a further drop in body temperature in AOAA treated mice. Even though tolerance to ethanol-induced hypothermia was present in ethanol-dependent mice, AOAA administration was able to produce a further decrease in body temperature. Bicuculline potentiated ethanol-induced hypothermia in the acute studies but the tolerance to hypothermia which had developed in ethanol-dependent mice prevented the bicuculline-induced potentiation of ethanol hypothermia. AOAA markedly potentiated acute ethanol-induced motor incoordination whereas bicuculline had no effect. Although partial tolerance had developed to ethanol-induced motor incoordination in dependent mice, AOAA potentiated, whereas a lower dose of bicuculline antagonized, motor incoordination. In the acute studies ethanol had a biphasic effect on AOAA-induced GABA accumulation in the hypothalamus and corpus striatum: low doses prevented and a slightly higher dose was without effect on GABA accumulation. Ethanol-dependent mice were unable to respond to an AOAA-induced increase in GABA accumulation although basal levels of GABA were unaffected by chronic ethanol ingestion. The results show that brain GABA or GABA-mediated central mechanisms may be involved in the mediation of ethanol-induced motor incoordination but not hypothermia.
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PMID:GABA mediation of the central effects of acute and chronic ethanol in mice. 403 3

The present study provides systematic evidence indicating a direct relationship between environmental temperature, rectal temperature and ethanol lethality. Male, C57 BL/6J mice, previously housed at room temperature (23 +/- 1 degree C), were injected intraperitoneally with 4.8 to 9.2 g kg-1 ethanol and then exposed for 24 h to ambient temperatures that did not appreciably exceed the thermally neutral range for sober mice (20 to 35 degrees C). There was a direct relationship between temperature and ethanol lethality at 8 and 24 h after injection. The 8 h LD50 increased by 64%, from 5.3 to 8.7 g kg-1, as environmental temperature decreased from 35 to 20 degrees C. The 24 h LD50 increased by 51%, from 5.3 to 8.0 g kg-1, across this temperature range. Each 5 degrees C reduction in ambient temperature induced a significant decrease in the rectal temperature of ethanol-injected mice. Mean rectal temperature ranged from 2.2 degrees C above baseline at an ambient temperature of 35 to 15 degrees C below baseline in the 20 degrees C environment. Ethanol induced a significant dose-related hypothermia in mice exposed to the 20, 25 and 30 degrees C environments but did not produce hypothermia in animals kept in the 35 degrees C environment. These findings indicate that the potency of potentially lethal ethanol doses varies with body temperature in accordance with partition and membrane expansion-fluidization theories of anaesthesia.
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PMID:Temperature dependence of ethanol lethality in mice. 613 99

A prominent effect of ethanol is on rectal body temperature. The use of a rectal probe to measure temperature can be stressful to the subject, especially when used repeatedly. We now present data on the hypothermic effect of ethanol (0.5, 1.0, 3.0, 3.5, or 4.0 g/kg) on surface body temperature in rats as detected by infrared radiation. Ethanol produced significant decreases in nasal temperature that were significantly correlated with changes in rectal temperature. Ethanol (3.5 g/kg) also produced a significant reversal in nasal hypothermia 15 min postinjection that was detected only with the infrared method. This new method is very rapid, accurate, requires minimal handling and may, therefore, be less stressful than rectal measurement to the subject.
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PMID:Effect of ethanol on surface body temperature as measured by infrared radiation detection. 641 14

The actions of indomethacin on the effects produced by ethanol were determined in rats and mice by measuring motor coordination (Rotorod test), sleep times, and body temperatures. Mice receiving indomethacin in combination with ethanol slept shorter times than those receiving ethanol alone. The blood and brain ethanol concentrations at time of awakening were significantly higher in the mice receiving the combination of drugs. Ethanol actions on motor impairment in rats and mice and on hypothermia in mice were not altered by pharmacologically relevant doses of indomethacin. The data show that indomethacin antagonizes only some of the observed effects of ethanol. It is suggested that a common mechanism, such as prostaglandin synthesis, is not involved in the interactions of both drugs.
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PMID:Ethanol and indomethacin interactions in motor impairment, hypnosis, and body temperature. 643 75

Ethanol-sensitive long-sleep mice showed greater sensitivity to ethanol-induced hypothermia whereas the less sensitive short-sleep mice showed greater sensitivity to morphine-induced hypothermia. The short-sleep mice, but not the long-sleep mice, displayed a degree of cross-tolerance to the hypothermic effects of ethanol following repeated exposure to morphine.
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PMID:Tolerance and cross-tolerance to morphine and ethanol in mice selectively bred for differential sensitivity to ethanol. 664 40

Hypothermia was studied 5 min before, and 30 and 60 min after intraperitoneal administration of ethanol (3 g/kg) in 20 inbred strains of mice. Ethanol was given daily for 8 days, and temperatures were taken on Days 1, 3, 5, and 8. Tolerance was indexed by the reduction in hypothermia over days. There were large strain differences in baseline temperature, the hypothermic effect of ethanol, and in development of tolerance to hypothermia. Some strains of mice (DBA/1J, DBA/2N, MA/MyJ, and PL/J) did not develop tolerance to the hypothermic effect of ethanol. Initial sensitivity to the hypothermic effect of ethanol was significantly genetically correlated with tolerance development, indicating control of these responses by common genes. Ethanol-induced changes in activity and ataxia, as well as blood ethanol concentrations, were also assessed. Although there were significant strain differences in activity reduction, ataxia, blood-ethanol concentrations, and changes in these parameters during the course of chronic treatment, none of these variables could explain the genetic differences in hypothermic sensitivity and tolerance.
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PMID:Tolerance to ethanol hypothermia in inbred mice: genotypic correlations with behavioral responses. 675 16

These experiments studied changes produced by a hypnotic dose of ethanol in the LS and SS lines of mice, which differ in ethanol sensitivity. In the first experiment, animals were injected either with ethanol or saline, and activity and seizure susceptibility measured 7-9 h later when blood levels of ethanol would have reached zero. Ethanol-treated mice of both genetic lines were less active in an open field test and more susceptible to clonic convulsions induced by flurothyl than saline-injected controls. There was no difference in the magnitude of these changes in the two lines. In the control condition SS (short-sleep) mice were more active than LS (long-sleep) mice, and more susceptible than LS mice to myoclonic but not to clonic seizures. The effect of the ethanol injection on body temperature was evaluated in separate groups of animals. LS mice showed a more pronounced hypothermia than SS mice when temperature was measured 2 h after injection. Six hours after injection, SS mice exhibited a small but statistically significant overshoot in temperature, after which they again became hypothermic with respect to controls; hyperthermia was not observed in LS animals.
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PMID:Withdrawal-like signs induced by a single administration of ethanol in mice that differ in ethanol sensitivity. 677 54

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

Ethanol ingestion has been implicated in accidental hypothermia of the elderly, but there is no prior data on the relative sensitivity to alcohol of aged homeotherms that might account for disproportionate dysthermia in this age group. To assess their sensitivity, ethanol (0.5-2.0 g/kg) or H20 was given by gavage to squirrel monkeys less than 4 yrs old, 4-9 yrs of age and over 9 yrs old. Dose-related decreases in body temperature occurred in all three groups in a 25.5 degrees C environment, with the greatest decreases in the oldest animals. In an 18.5 degrees C environment the hypothermias caused by 0.5 and 1.0 g/kg ethanol were greatly augmented in old monkeys and in some cases their temperatures fell to potentially life-threatening levels. In a 30.5 degrees C environment, 1.0 g/kg ethanol given to monkeys caused approximately equal temperature reductions in the three groups. When determined after 1.0 g/kg ethanol, peripheral vasomotor tone increased significantly in animals of each age group in all three environments. Decreases in rectal temperature were associated with parallel decreases in oxygen consumption. These results indicate that: 1) aging is associated with an increased sensitivity to the hypothermic action of ethanol in thermoneutral and cold environments, 2) ethanol in the doses tested inhibits heat production mechanisms without suppressing compensatory vasoconstriction in response to decreased body temperature.
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PMID:Effects of alcohol on thermoregulation in aged monkeys. 687 10

Ethanol (0.5-3.2g x kg-1 i.p.) caused a dose-dependent fall in body temperature in rats. A dose of 1.5g x kg-1 i.p. led to a fall of 1.6 +/- 0.20 degrees C over 60 min at an environmental temperature of 18 +/- 1 degrees C. There was no evidence of acute tolerance when the hypothermic response was elicited by the same dose of ethanol (0.7--20.0g x kg-1 i.p.) 24 h later; indeed the second response was consistently, although not significantly, greater than the first. Behavioral thermoregulatory studies indicated that the fall in temperature after ethanol is due, at least in part, to a downward setting in the thermoregulatory set point. These results suggest that the rat may be a suitable animal model for a study of accidental hypothermia following ethanol ingestion and exposure to low environmental temperatures.
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PMID:Ethanol-induced hypothermia in the rat. 742 11


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