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

The time course of the effects of ethanol alone and in combination with the selective alpha 2-adrenoceptor agonist dexmedetomidine and the alpha-adrenoceptor antagonist atipamezole was studied in NIH-Swiss mice. Core body temperature, rotarod performance, motility and changes in the noradrenaline, dopamine, and 5-hydroxytryptamine (5-HT) metabolite contents of different brain parts (limbic forebrain, striatum, lower brainstem, the rest of the forebrain + midbrain and hypothalamus) were measured. Atipamezole (3 mg/kg) attenuated the hypothermia induced by either ethanol (3 g/kg) alone or ethanol in combination with dexmedetomidine (0.3 mg/kg). Atipamezole shortened the duration of the ethanol-impaired and ethanol + dexmedetomidine-impaired rotarod performance. Further, atipamezole prevented the decreased motility due to the combined treatment with ethanol and dexmedetomidine. Ethanol increased 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) values. Dexmedetomidine alone decreased MHPG and 5-hydroxyindoleacetic acid (5-HIAA) concentrations and increased DOPAC and HVA values. Dexmedetomidine combined with ethanol resulted in a further increase in DOPAC and HVA values. Pharmacokinetic parameters did not contribute to this antagonism of ethanol's effects by atipamezole, nor did the antagonism observed in rotarod performance or hypothermia seem to correlate with the changes seen in the brain noradrenaline and dopamine or 5-HT metabolism. In conclusion, these findings suggest that several ethanol effects are not mediated via direct activation of alpha 2-adrenoceptors, even though some of ethanol's behavioral and physiological effects may be antagonized by coadministration of alpha 2-adrenoceptor antagonists.
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PMID:The effects of ethanol in combination with the alpha 2-adrenoceptor agonist dexmedetomidine and the alpha 2-adrenoceptor antagonist atipamezole on brain monoamine metabolites and motor performance of mice. 753 79

The hypothermic action of ethanol was investigated in genetically distinct lines of mice selected for sleep-time response to pentobarbital for six generations. Ethanol (3 g/kg, intraperitoneally) was administered to alcohol-naive males and females from each of the unselected control, long-, and short-sleep mouse lines. Rectal temperatures were measured immediately before, and at 15, 30, 60, 90, 120, and 240 min after ethanol injection. Eight female and eight male mice from each line were sacrificed at each time point, and trunk blood was collected for plasma ethanol analysis. The results show that short-sleep mice were less hypothermic (p < 0.05) compared to long-sleep mice at 15 and 30 min after ethanol administration. However, plasma ethanol concentrations were not significantly different between the mouse lines at any time point. Therefore, the line-dependent differential ethanol-induced hypothermia observed may be a result of differences in "brain sensitivity" rather than in the rates of ethanol metabolism among the mouse lines.
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PMID:Hypothermic effect of ethanol in mice selected for differential sleep-time response to pentobarbital. 766 80

Because tacrine, a cognitive enhancing agent, was being considered for approval for use in Alzheimer's disease, its possible interaction with ethanol, a commonly used substance to which elderly individuals are generally more sensitive than younger individuals, was explored. For purposes of comparison, two other drugs, which have also been shown to improve memory in mice, at doses which had activity in a working memory paradigm, were evaluated for an interaction with ethanol. Ethanol-induced sedation in mice was increased by tacrine and decreased by physostigmine, whereas AIT-082 did not alter sedation. However, tacrine had no effect on body temperature or on ethanol-induced hypothermia. Neither tacrine nor physostigmine had any effect on the rate of ethanol elimination from the blood. As tacrine comes into clinical use in the treatment of Alzheimer's disease, adverse interactions with ethanol should be explored further.
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PMID:The interaction of ethanol with the cognitive enhancers tacrine, physostigmine, and AIT-082. 812 46

The postnatal development of certain neurochemical correlates of CNS ethanol sensitivity was examined in the long-sleep (LS) and short-sleep (SS) mice. The differences in sensitivity to the motor-incoordinating and hypothermic effects of ethanol emerged during the second and third weeks of life. Prior studies have shown the sleep time differences between LS and SS mice became significant at 8-10 days of age whereas the present results established that the differences in ethanol-induced hypothermia became prominent at 12-16 days of age. Previous results from our laboratory suggested that the greater CNS ethanol behavioral sensitivity (sleep time and hypothermia) of LS mice is related to the greater ethanol-induced depression of brain monoamine synthesis in the LS line. The timing of the developmental changes in neurochemical ethanol sensitivity in LS and SS mice was found to parallel that found in the development of behavioral ethanol sensitivity as follows. Ethanol-induced decreases in in vivo tyrosine hydroxylase activity in the cerebellum, hypothalamus, and brain stem did not differ between LS and SS mice at postnatal day 8, but became substantially greater in LS mice between postnatal days 8 and 12, coincident with the appearance of the greater sleep times of LS mice. Likewise, ethanol-induced decreases in in vivo tryptophan hydroxylase activity in the dorsal raphe and hypothalamus, which were similar in LS and SS mice at postnatal days 8 and 12, became significantly greater in LS mice by postnatal day 16, the age at which their increased sensitivity to ethanol-induced hypothermia appeared.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of neurochemical and behavioral sensitivity to ethanol in long-sleep and short-sleep mice. 851 37

We compared some biobehavioral effects of ethanol in transgenic mice that overexpress insulin-like growth factor I (IGF-I) in brain and in those that exhibit ectopic: brain expression of IGF binding protein I with those in non-transgenic littermate controls. Ethanol-induced sleep in IGF-I transgenic mice was significantly shorter, and in IGF binding protein 1 transgenic mice significantly longer, than in controls. A similar tendency, though not significant, was observed for ethanol-induced hypothermia. The groups did not differ in the degree of ethanol-induced ataxia. IGF-I transgenic mice did not acquire tolerance to either the hypothermic or hypnotic effects of ethanol following 7-day ethanol treatment. In contrast, tolerance in IGF binding protein 1 transgenic mice was significantly more pronounced than in controls. There were no significant differences among the three groups in the peak blood alcohol concentrations or the overall blood alcohol curves following acute ethanol challenge. In general, these data support the prediction made that chronically elevated exposure to IGF-I in IGF-I transgenic mice renders them less susceptible to the effects of ethanol than their non-transgenic siblings, and that overexpression of IGF binding protein 1 has the opposite effect.
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PMID:Insulin-like growth factor I expression alters acute sensitivity and tolerance to ethanol in transgenic mice. 881 32

Hypothermia and ethanol are often closely linked and in hypothermic accidents ethanol is often a contributing factor. To study the effects of ethanol on the circulation in hypothermic conditions, cardiac catheterization was carried out on 18 anaesthetized beagle dogs. They were divided into two groups. One gram of ethanol/kg of b.wt. diluted in saline was infused into the vena cava superior within 30 min to seven dogs. The dogs were then cooled between ice bags until the blood temperature in the ascending aorta was 25 degrees C and they were then rewarmed. The control group of 11 dogs was cooled and rewarmed without ethanol infusion. The heart rate first increased when cooling down to 33 degrees C and decreased thereafter in the control group. In the ethanol group heart rate increased during the ethanol infusion and remained high when cooling down to 33 degrees C and decreased thereafter. Heart rate was higher in the ethanol group throughout the experiments, and during rewarming the difference was significant. In the control group cardiac output first increased until a body temperature of 33 degrees C was achieved but then decreased. In the ethanol group cardiac output started to decrease after ethanol infusion. During rewarming there was a significantly higher cardiac output in the ethanol group, probably due to the higher heart rate. In the cardiac cycle the systolic period prolonged significantly (p < 0.001) in both groups when the body temperature decreased from 37 degrees C to 25 degrees C whereas the diastolic period remained quite stable. The contraction phase was also affected by the cooling. The changes in contraction force cannot be seen in dP/dt alone because dP/dt values first increased significantly when cooling from 37 degrees C to 33 degrees C but then decreased. Ejection fraction, systolic period, and the systemic vascular resistance increased despite the reduction of the dP/dt and thus we conclude that the contraction force is augmented in hypothermia. In the ethanol group the myocardium seems to be depressed due to ethanol. In the early phase of cooling heart rate increased but cardiac output decreased in the ethanol group, indicating the decreased ability of the heart to respond to cooling in the presence of ethanol. The time constant of exponential pressure fall (tau) increased linearly with cooling from 37 degrees C to 25 degrees C and recovered with rewarming in both groups. Changes in negative dP/dt coincided with the changes in the time constant of exponential isovolumic pressure fall. Ethanol did not influence relaxation. All the parameters we checked recovered to normal during rewarming.
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PMID:Influence of ethanol on circulation in surface-induced hypothermia and subsequent rewarming. 881 44

Several previous studies have shown that 1 to 2 weeks of treatment with ethanol elicits tolerance to several effects produced by ethanol and cross-tolerance to nicotine-induced hypothermia. Similarly, short-term, high-dose nicotine treatment produces tolerance to nicotine and cross-tolerance to ethanol-induced hypothermia. In the studies reported here, C57BL/6 mice were force-fed ethanol, nicotine, or an ethanol/nicotine combination in the drinking water for 6 months. All of the chronic drug-treated mice developed tolerance to ethanol as measured by open-field activity, body temperature, and sleep-time tests. Ethanol tolerance is due, in part, to enhanced metabolism and reduced CNS sensitivity in the two ethanol-treated groups but only to reduced CNS sensitivity in the nicotine-treated group. Similar levels of tolerance to nicotine developed in those two groups that were nicotine-treated, but no tolerance to nicotine was seen in those animals treated with ethanol alone. The tolerance to nicotine may be related to an upregulation of brain (cortex, hippocampus, and hypothalamus) [3H]-nicotine binding, but ethanol tolerance is not readily explained by changes in the number of the brain high affinity nicotine binding sites.
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PMID:Long-term ethanol and nicotine treatment elicit tolerance to ethanol. 889 17

Peripheral administration of selective agents for GABAA receptors have been reported to modify ethanol self-administration behaviour. Recently, it has been reported that the dorsal and median raphe may represent potential brain sites for mediating these effects since injection of the GABAA agonist, muscimol, into these sites increased ethanol intake. The aim of the present study was to extend these findings and assess the effect of muscimol, injected into either the dorsal or median raphe, on a range of parameters including ethanol intake, ethanol-induced hypothermia and ethanol-induced suppression of high rates of responding. Wistar rats trained to drink 12% ethanol for 40 mins each day, increased their ethanol consumption, but not water consumption, following injection of 50 ng muscimol into the dorsal raphe. Ethanol intakes returned to baseline levels the day following drug treatment. The same dose injected into the median raphe has been shown to produce a non-selective increase in both water and ethanol intake. Further analysis of this data revealed that the rats tended to avoid the ethanol solution on the day following treatment. A further difference between the dorsal and median raphe was revealed in the ethanol-induced hypothermia experiment. Thus, 10 ng muscimol injected into the median raphe potentiated the hypothermic response induced by intraperitoneal injection of 1.5 g/kg ethanol, whereas injection into the dorsal raphe had no significant effect on this measure. Intraperitoneal injection of 0.5 g/kg ethanol suppressed operant responding for water intake and this behaviour was not altered by dorsal raphe injection of muscimol. Together these results suggest that GABAergic mechanisms within the dorsal raphe represent an important neural site for controlling the ingestion of ethanol, but not that of ethanol intoxication.
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PMID:Effect of dorsal raphe injections of the GABAA agonist, muscimol, on ethanol intake and measures of intoxication in Wistar rats. 897 82

The effects of the GABAA receptor antagonists, pentylenetetrazol, bicuculline, and picrotoxin, the glycine antagonist, strychnine, and the NMDA receptor antagonist, memantine, on ethanol-induced behavioral sleep and body temperature were investigated. Pentylenetetrazol, bicuculline, and picrotoxin given prior and following ethanol reduced the behavioral sleep and potentiated the hypothermia caused by ethanol. However, convulsions appeared when bicuculline, but not pentylenetetrazol and picrotoxin, were given following ethanol. After the reversal of unconsciousness in rats without convulsions the animals remained awake throughout the experiments without motor incoordination, hyperexcitability, and sedation, but they were in hypothermia within 12 h. The glycine antagonist, strychnine, given prior or after ethanol had virtually no effect on ethanol-induced behavioral sleep and hypothermia. Ethanol given prior or following strychnine failed to antagonize strychnine-induced convulsions. The NMDA receptor antagonist, memantine, given following ethanol potentiated the behavioral sleep and had virtually no effect on hypothermia induced by ethanol. It is suggested that the ethanol-induced behavioral sleep may be attributed to its ability to enhance the GABAergic mechanisms and to inhibit NMDA-mediated excitatory responses. However, the ethanol-induced hypothermia may be ascribed solely to the facilitation of GABAergic transmission. Further, it is postulated that a bidirectional inhibitory system subserves the regulation of behavioral sleep and convulsions. However, one-way inhibitory system underlies the ethanol-induced hypothermia.
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PMID:Opposite effects of GABAA and NMDA receptor antagonists on ethanol-induced behavioral sleep in rats. 908 18

The effect of dexamethasone on ethanol-induced hypothermia was investigated in 3.5-month old male Wistar rats (N = 10 animals per group). The animals were pretreated with dexamethasone (2.0 mg/kg, i.p.; volume of injection = 1 ml/kg) 15 min before ethanol administration (2.0, 3.0 and 4.0 g/kg, i.p.; 20% w/v) and the colon temperature was monitored with a digital thermometer 30, 60 and 90 min after ethanol administration. Ethanol treatment produced dose-dependent hypothermia throughout the experiment (-1.84 +/- 0.10, -2.79 +/- 0.09 and -3.79 +/- 0.15 degrees C for 2.0, 3.0 and 4.0 g/kg ethanol, respectively, 30 min after ethanol) but only the effects of 2.0 and 3.0 g/kg ethanol were significantly antagonized (-0.57 +/- 0.09 and -1.25 +/- 0.10, respectively, 30 min after ethanol) by pretreatment with dexamethasone (ANOVA, P < 0.05). These results are in agreement with data from the literature on the rapid antagonism by glucocorticoids of other effects of ethanol. The antagonism was obtained after a short period of time, suggesting that the effect of dexamethasone is different from the classical actions of corticosteroids.
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PMID:Ethanol-induced hypothermia in rats is antagonized by dexamethasone. 922 6


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