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

Effects of selective alpha 2-adrenoceptor antagonists, atipamezole and idazoxan, on ethanol-induced hypothermia were investigated in mice. Ethanol significantly reduced (P less than 0.001) core temperature whilst both alpha 2-adrenoceptor antagonists were without effect when administered alone. However, both the 1 and 3 mg/kg doses of atipamezole significantly (P less than 0.05) attenuated the ethanol-induced reduction in body temperature 20 and 40 min after administration. The 3 mg/kg dose of idazoxan (but not the 1 mg/kg dose) also significantly (P less than 0.05) attenuated ethanol's hypothermic effect 20 min after administration but this effect was not statistically significant at 40 min. In a subsequent experiment using lower doses of atipamezole (0.03-1.0 mg/kg) the attenuation of ethanol-induced hypothermia caused by atipamezole was found to be dose-related. The effect of the benzodiazepine inverse agonist Ro 15-4513 on ethanol-induced hypothermia was also investigated. This compound possessed an intrinsic hypothermic action but neither attenuated nor enhanced the hypothermic effect of ethanol. These results suggest that alpha 2-adrenoceptor can, at least partially, modulate the hypothermic effects of ethanol.
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PMID:Attenuation of hypothermic effects of ethanol by alpha 2-adrenoceptor blockers. 257 27

Effects of acute or chronic ethanol administration have been studied on protein, RNA and DNA synthesis in the developing brain in the absence or presence of hypothermia. Acute ethanol was given intraperitoneally (4 g/kg) and for chronic ethanol treatment the pups were allowed to suckle on the ethanol-fed dams. Dams were pair-fed on nutritionally adequate liquid-sustacal diet. Ethanol administration, both acutely and chronically, inhibited the in vivo and in vitro protein synthesis in the absence or presence of hypothermia. This data suggests that ethanol per se is capable of producing the inhibition of protein synthesis in brain without its hypothermic effect. However, the inhibitory effect of ethanol is more pronounced in the presence of ethanol-mediated hypothermia. Hypothermia in itself also causes a decrease in the synthesis of proteins. Maternal ethanol consumption results in a significant decrease in the synthesis of both RNA and DNA in the developing brain of suckling newborn either in the absence or presence of hypothermia. RNA and DNA synthesis was measured by following the incorporation of (5-(3)H) uridine and (14C)thymidine respectively. Decrease in body temperature alone also resulted in decreased RNA and DNA synthesis in the developing brain. Ethanol reaching the suckling newborn from maternal milk resulted in decreased brain weights, total protein, ribosomal protein, total RNA, ribosomal RNA, and total DNA of the brain. Neonatal brain proteolytic and DNA-polymerase activities were inhibited in the ethanol-fed group. An inhibition of proteolytic activity reflects a compensatory mechanism of the developing brain to decrease the breakdown of proteins in response to the inhibitory effect of ethanol on protein synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nucleic acid and protein synthesis inhibition in developing brain by ethanol in the absence of hypothermia. 258 87

Ethanol, i.p., produced a greater dose-dependent hypothermia in long sleep (LS) than in short sleep (SS) mice with significant decreases in rectal temperature observed only at doses greater than 3 g/kg, i.p. Likewise, at doses of 1 to 2 g/kg ethanol, i.p., these lines of mice differ markedly in locomotor activity. Neurotensin (NT), intracerebroventricular (I.C.V.), induced a similar hypothermia in both SS and LS mice at doses greater than 0.02 microgram. Doses of ethanol (1.0 g/kg) or NT (0.005 microgram, i.c.v.) that failed to cause hypothermia when administered separately produced a pronounced hypothermia when administered together. Potentiation of NT and ethanol-induced hypothermia was greater in SS than in LS mice. Sensitivity to NT-induced hypothermia was greater following i.c.v. administration than by infusion into the nucleus accumbens (NA) or the ventral tegmental area (VTA). Neurotensin, i.c.v. or intra-NA, markedly inhibited ethanol-induced increase in locomotor activity in both SS and LS mice; however, NT, intra-VTA, did not alter the effects of ethanol on locomotor activity. The results suggest that NT and ethanol act in a synergistic manner on specific neuronal processes mediating thermoregulation and spontaneous motor activity.
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PMID:Neurotensin and ethanol interactions on hypothermia and locomotor activity in LS and SS mice. 264 82

A suitable model for the study of the interaction of the aging process and prolonged treatment with ethanol is described. Animals were given 15% ethanol in the drinking water for up to 25 months. There was little disruption in the growth of the animals. Ethanol treatment resulted in a number of neurological and morphological changes some of which persisted throughout the treatment period. Both young and old animals displayed metabolic tolerance by the criteria of resistance to ethanol-induced hypothermia and increased metabolism of [14C]ethanol. The regime used has proved useful in the study of the interaction of ethanol and aging in the rat.
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PMID:A feeding regime for the study of the interaction of ethanol and aging. 270 28

The effects of microinjections of thyrotropin-releasing hormone (TRH), neurotensin and ICI 174864 into the nucleus accumbens, nucleus caudatus, septum and mesencephalic periaqueductal grey were studied on ethanol-induced narcosis in the rat. Levels of narcosis were assessed by alterations in ethanol-induced hypothermia and sleep time. Ethanol produces a 2 degree C fall in body temperature over the first hour which then recovered over the next 2 h. Sedation was produced to the extent that the righting reflex was lost for between 80 and 90 min. In the nucleus caudatus all 3 peptides were ineffective at altering narcosis. In the periaqueductal grey, septum and accumbens, TRH (5 micrograms) and ICI 174864 (1 microgram) microinjections significantly reduced the sleep time by between 50 and 70%. ICI 174864 was approximately 10 times more potent that TRH at reducing the sleep time. In addition, both these peptides significantly accelerated the recovery from the ethanol-induced hypothermia in the periaqueductal grey, septum and accumbens. ICI 174864 prevented the ethanol-induced fall in body temperature. Neurotensin (5 micrograms) significantly increased the sleep time by up to 50% and potentiated the ethanol-induced hypothermia. These results suggest that the administration of TRH or the blockade of delta-opioid receptors, resulting in an inhibition of endogenous enkephalin transmission, may significantly inhibit ethanol narcosis in the rat. Opposing this, the application of neurotensin appears to potentiate ethanol narcosis. These results also indicate that endogenous enkephalin release plays an important role in ethanol narcosis.
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PMID:The effect of neurotensin, TRH and the delta-opioid receptor antagonist ICI 174864 on alcohol-induced narcosis in rats. 282 97

The effect of hypothermia (29 C) on the pharmacokinetics of ethanol was studied in eight piglets serving as their own normothermic controls. Ten milliliters of 12% ethanol per kilogram were infused over 30 minutes, and serum ethanol concentrations were measured for seven hours. Ethanol concentration data were fitted to one-compartment open model assuming Michaelis Menten elimination kinetics. During hypothermia, ethanol concentrations were consistently higher than during normothermia. This observation could be explained by both a significantly smaller distribution volume of ethanol during hypothermia (0.71 +/- 0.03 L/kg at 29 C and 0.84 +/- 0.05 L/kg at 37 C, P less than .02) and a significantly slower maximum velocity of metabolism of ethanol (Vm) during hypothermia (1.12 +/- 0.11 mg/kg.min vs. 1.83 +/- 0.21 mg/kg.min, P less than .01). Our study indicates that during hypothermia, ethanol stays significantly longer in the circulation in piglets. Potentially, this may contribute to a more profound effect from the ethanol.
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PMID:Effect of hypothermia on the pharmacokinetics of ethanol in piglets. 291 73

LS/Ibg (LS) and SS/Ibg (SS) mice differ in ethanol-induced duration of loss of righting response or sleep time, hypothermia, hyperglycemia, and blood ethanol concentrations at regaining righting response. These differences in response to ethanol are a result of differences in central nervous system sensitivity and are mediated by polygenic systems. Studies have indicated that catecholaminergic systems may be involved in the differential effects of ethanol in LS and SS lines of mice (Masserano JM, Weiner N: Investigations into the neurochemical mechanisms mediating differences in ethanol sensitivity in two lines of mice. J Pharmacol Exp Ther 221:404-408, 1982). In this study the neurotoxin, 6-hydroxydopamine (6-OHDA), intracerebroventricular, was used to test this hypothesis. Administration of 6-OHDA markedly altered thermoregulation in LS mice but produced little effect in SS mice, and ethanol-induced hyperglycemia was attenuated in both LS and SS mice by 6-OHDA. Ethanol-induced sleep time was increased in SS mice pretreated with 100 micrograms of 6-OHDA, intracerebroventricular, whereas this response in LS mice was unaffected by 6-OHDA administration. Changes in sleep time were not related to changes in blood ethanol concentrations, indicating that 6-OHDA alters ethanol-induced sleep time by mechanisms other than brain sensitivity. Levels of norepinephrine and dopamine were determined in three brain regions, and the altered capacities for thermoregulation and glucoregulation were associated with changes in hypothalamic catecholamine levels.
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PMID:Effects of 6-hydroxydopamine on brain catecholamines and on acute actions of ethanol in LS/Ibg and SS/Ibg mice. 309 Sep 1

This study deals with the interaction between high pressure and a sub-hypnotic dose of ethanol in rats. Male Sprague-Dawley rats were given either ethanol 1.5 g/kg or saline IP and subsequently exposed to 1 atmosphere absolute pressure (ATA) air or to 1, 12, 24 or 48 ATA of helium-oxygen (heliox). The gas temperature was adjusted to offset ethanol and helium-induced hypothermia. Ethanol induced a characteristic unsteady pattern of locomotion which was completely reversed at 48 ATA, partially reversed at 24 ATA, but not affected at 12 ATA. Other behavioral effects of ethanol such as depression of total motor activity and rearing were similarly affected. Blood and brain concentrations of ethanol in the pressure groups did not differ significantly from concentrations measured in the 1 ATA groups. A similar pattern of reversal was observed whether the compression was initiated 4, 10 or 16 min after injection. These results show that hyperbaric exposure antagonizes the depressant effect of ethanol on spontaneous behavior in rats. This antagonism does not appear to be due to changes in ethanol distribution or elimination.
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PMID:Pressure reversal of the depressant effect of ethanol on spontaneous behavior in rats. 335 18

The initial sensitivity to ethanol was determined by hypothermia and sleeping time induced by an injection of ethanol (2.5 g/kg, intraperitoneally) in Long-Evans rats whose response to ethanol was later characterized in drinking, non-drinking and other rats. The response to a nociceptive stimulus (electric shock) in drinking rats and non-drinking rats was also studied. There was no correlation between initial sensitivity to ethanol and ethanol consumption and all rats exhibited the same behaviour towards electric shock. Ethanol elimination was not significantly different in both groups after an i.p. injection of a 2.5 g/kg dose of ethanol. These data indicate that our selected drinking and non-drinking rats differ in their ethanol intake behaviour but not in their initial sensitivity to ethanol or their sensitivity to a nociceptive stimulus. Preference for, and initial sensitivity to, ethanol are therefore not related in our rats.
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PMID:Is initial sensitivity to ethanol correlated with alcohol preference in alcohol-drinking and non-drinking rats? 342 70

We investigated whether thiamine deficiency (TD), a frequent concomitant of chronic alcoholism, differentially modifies the response to ethanol in two inbred rat strains with highly different genetic susceptibilities to development of TD encephalopathy. Ethanol-induced (3 g/kg i.p.) behavioral impairment and hypothermia were studied after 2, 5 and 7 weeks of TD and after 6 weeks of repletion on normal diet. Controls of the M520/N (TD-sensitive) strain metabolized ethanol more rapidly, had a greater liver to body weight ratio, greater total body water, earlier and lower peak blood ethanol concentrations (BEC), diminished area under the BEC curve and lesser behavioral impairment and hypothermia (even at equivalent BEC values) than those of the F344/N (TD-resistant) strain. In both strains, TD resulted in reduced ethanol metabolic rate and liver to body weight ratio and equivalent ethanol-induced hypothermia and behavioral impairment at lower BEC. Lower and delayed peak BEC and unchanged area under the BEC curve suggest an increased volume of ethanol distribution during TD. Recovery appeared complete after 6 weeks of normal diet. Both strains lost an equivalent proportion of body weight during TD but M520/N rats had lesser decrements in ethanol metabolic rate, had greater reductions in liver weight, peak BEC and baseline body temperature and developed overt encephalopathy whereas F344/N rats did not. Therefore, in the chronic alcoholic, TD may modify ethanol's effects via pharmacokinetic and pharmacodynamic mechanisms. Relatively high ethanol tolerance of the strain with a genetic predisposition to TD encephalopathy is consistent with the hypothesized role of this avitaminosis in the pharmacogenetics of alcoholism.
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PMID:Influence of thiamine deficiency on the response to ethanol in two inbred rat strains. 355 71


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