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

The development of tolerance to ethanol-induced hypothermia and hypnosis, and cross-tolerance with morphine was studied in mice and rats. Ethanol significantly decreased the body temperature in rats (3.0 and 3.2 g/kg) and in mice (3.5 and 4.0 g/kg). Chronic administration of ethanol resulted in the tolerance not only to ethanol hypothermia but also to hypothermic effects of morphine in examined animals. Implantation of morphine pellets caused the development of cross tolerance to ethanol-induced hypothermia in rats but not in mice. The hypnotic effect of ethanol was significantly shorter in chronic alcoholized rats but not in morphine-implanted rats. Neither chronic ethanol administration nor implantation of morphine pellets changed the duration of ethanol-induced hypnosis in mice. These results seem to support the hypothesis on the opiate-like mechanism of ethanol action.
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PMID:Ethanol-induced hypothermia. Cross tolerance with morphine. 359 59

Single doses of d-amphetamine, chlorpheniramine or diazepam were combined with ethanol under two conditions: (i) in drug-naive mice and (ii) in mice which had been given a single dose of ethanol 72 hr previously. Ethanol was administered orally at doses of 6.0, 3.0 or 1.5 g/kg; doses of d-amphetamine, chlorpheniramine or diazepam were given intraperitoneally. Three parameters were measured; changes in rectal temperature, forced motor coordination, as evaluated by rotarod performance and concentrations of ethanol in blood. d-Amphetamine and chlorpheniramine attenuated the hypothermia induced by ethanol but had no effect on the motor-impairing effect of ethanol. Hypothermia induced by diazepam was unaffected by ethanol, but the combination appeared to impair maximally rotarod performance. Concentrations of ethanol in blood did not differ between ethanol-naive mice and mice which had received the same dose of ethanol 72 hr previously. Changes in body temperature and intoxication have been attributed to central actions of ethanol; however, the differential results obtained from the interactions between these drugs suggest differing sensitivities of the various systems which are affected by ethanol.
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PMID:Drug interactions with ethanol. Effects on body temperature and motor impairment. 370 79

Ethanol has been shown to induce a hypothermia in rats maintained in air at 26 degrees C. The objective of the present study was to assess the metabolic responsiveness of ethanol-treated rats to administration of isoproterenol, a beta-adrenoceptor agonist, and to assess whether ethanol per se, or the hypothermia accompanying its administration, contribute to changes in beta-adrenergic responsiveness. In the present study, administration of ethanol (3 g/kg, i.p.) reduced both colonic temperature (Tco) and rate of oxygen consumption (metabolic rate) of rats maintained at 26 degrees C to levels below those of saline-treated controls within 20 min after treatment. Maximal decreases in both parameters occurred within approximately 40 min. Administration of isoproterenol (50 micrograms/kg, s.c.) 10 min after treatment with either ethanol or saline was accompanied by an increase in the metabolic rates of both groups, although the magnitude of the increase in the ethanol-treated group was less than that of controls. Maximal increases in tail skin temperatures (Tsk) following treatment with isoproterenol were similar in both groups but an increase in Tsk occurred earlier in the ethanol-treated group. Tco increased after treatment with isoproterenol in the saline-treated group but decreased in the ethanol-treated group. When isoproterenol was administered 90 min after treatment with ethanol, increases in metabolic rate, Tsk, and Tco were similar in both groups, although the increase in Tsk of ethanol-treated animals was delayed until Tco reached pretreatment level. Exposure to 30 degrees C minimized ethanol-induced hypothermia. At this temperature the metabolic responses to administration of isoproterenol at 90 min after treatment with ethanol did not differ significantly between the two groups. These results suggest that the metabolic responsiveness to administration of a beta-adrenoceptor agonist is not altered by prior treatment with ethanol but is affected by the hypothermia accompanying its administration.
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PMID:Beta-adrenergic responsiveness in the rat following acute administration of ethanol. 371 5

Adult guinea-pigs were treated with ethanol (2.5 g/kg, IP) or acetaldehyde (100 mg/kg, IP) and exposed to moderate cold (+4 degrees C) for 50 minutes. Controls were given 0.9% NaCl solution. The hypothalamic catecholamines norepinephrine (NE) and dopamine (DA) and also norepinephrine and epinephrine (E) in the serum were analyzed by high-performance liquid chromatography with an electrochemical detector. Blood glucose, free fatty acids and glycogen in the liver and skeletal muscle were also measured. Acetaldehyde caused a similar drop in colon temperature as did ethanol, but neither could prevent cold-induced vasoconstriction in the ear lobe. Ethanol significantly reduced the concentration of NE in the hypothalamus compared to the controls. Acetaldehyde had a tendency to lower hypothalamic NE. There was no significant difference between drug-treated groups in NE concentration. Neither ethanol nor acetaldehyde had any effect on hypothalamic DA. In the ethanol group serum E and glucose were significantly elevated compared to the acetaldehyde group. Serum glucose was also higher compared to the controls, and the difference in serum E concentration near the level of significance. No significant differences were found between the groups in serum NE, FFA or skeletal muscle and liver glycogen concentration. The results point to a possible central effect of ethanol during a short-term moderate cold exposure. The effects of acetaldehyde on neuronal tissue remain speculative, but a possible effect on noradrenergic neurons cannot be ruled out. Although the hypothermic effect of acetaldehyde corresponded that of ethanol, further experiments are required to elucidate the role of acetaldehyde in ethanol-induced hypothermia.
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PMID:Hypothalamic and serum catecholamines in ethanol and acetaldehyde treated guinea-pigs. Relation to moderate short-term cold exposure. 381 45

Evidence is reviewed linking clinical effects of ethanol with actions on the sympathetic and parasympathetic nervous systems. The studies reported include a series of investigations by the authors. Acutely, ethanol causes peripheral vasodilation and may also result in changes in heart rate and blood pressure. Ethanol may contribute to acute problems which may present clinically, including micturition syncope, accidental hypothermia and facial flushing. However, increased sympathetic nervous activity plays a role in causing hypertension and other symptoms during ethanol withdrawal in chronic alcoholics. Some chronic alcoholics may have neuropathy involving sympathetic nerves, and this can result in distal sweating loss and occasionally in orthostatic hypotension. Also, hypothalamic lesions associated with Wernicke's encephalopathy may result in hypothermia. Neuropathy involving parasympathetic nerves in not uncommon in alcoholics with other evidence of nervous system damage, but it is generally asymptomatic. Occasionally, vagal neuropathy may cause disorder of gastrointestinal motility, and neuropathy affecting the sacral innervation may be a factor in alcoholic impotence.
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PMID:The effects of acute and chronic ingestion of ethanol on the autonomic nervous system. 381 27

Ethanol, administered i.p., produced a dose-dependent increase in plasma norepinephrine and epinephrine concentrations in LS/Ibg (LS) but not in SS/Ibg (SS) lines of mice. Ethanol-induced elevations of plasma epinephrine in LS mice were approximately 10-fold greater than those observed in SS mice. Plasma epinephrine and norepinephrine attained peak concentrations at 20-min post-ethanol administration at doses ranging from 2.8 to 4.1 g/kg. Plasma catecholamines remained elevated for approximately 1 hr and returned to basal values 2 hr after ethanol administration. Significant correlations were obtained between blood ethanol (r = 0.99), plasma epinephrine (r = 0.92) and plasma glucose (r = 0.98) as a function of ethanol dose in LS mice. Chlorisondamine (3 mg/kg), a ganglionic blocker, abolished completely the ethanol-induced increase in plasma catecholamines. These results confirm previous suggestions that the response is centrally mediated through an increased sympathetic outflow rather than by a direct effect on the adrenal medulla. The increase in plasma epinephrine and associated hyperglycemia produced by ethanol was not observed with pentobarbital or halothane anesthesia. Ethanol-induced hypothermia was diminished markedly (47%) by an elevated ambient temperature (28 degrees C) without reducing the hyperglycemic response to ethanol. These results suggest that ethanol-induced hypothermia does not mediate ethanol-induced adrenomedullary catecholamine secretion and concomitant hyperglycemia. It is proposed that the differential ethanol-induced secretion of adrenomedullary catecholamines in LS and SS mice is due to differential central nervous system sensitivities to ethanol.
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PMID:Ethanol-induced adrenomedullary catecholamine secretion in LS/Ibg and SS/Ibg mice. 395 Aug 66

Ethanol-induced intoxication and hypothermia were studied in rats approximately 7 months after severe thiamine deficiency, when treated rats appeared to have recovered their physical health. Previously induced thiamine deficiency without prior ethanol exposure significantly decreased the area under the curve plotted for the concentration of ethanol in blood and also decreased behavioral impairment and hypothermia due to ethanol exposure. Pathophysiologic changes resulting from thiamine deficiency may contribute to both the pharmacodynamic and pharmacokinetic tolerance to ethanol in chronic alcoholics.
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PMID:Response to ethanol reduced by past thiamine deficiency. 397 22

Administration of single doses of ethanol, 1-propanol, 1-butanol or 1-pentanol to mice caused hypothermia and impairment of rotarod performance. Repetitive doses, at 24-72 hr intervals led to development of tolerance to the hypothermic effects of ethanol but not of the other alcohols. No tolerance was seen in the impairment of rotarod performance with repeated doses of any of the alcohols. Ethanol did show an intersession tolerance on rotarod performance; at 20 and 80 min after injection, blood levels were similar, while performance was impaired at 20 but not at 80 min.
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PMID:Differing effects of short-chain alcohols on body temperature and coordinated muscular activity in mice. 398 4

The effects of D-methamphetamine HCl (1, 2 and 4 mg/kg, i.p.) and alpha-methyldopa (1, 2 and 4 mg/kg, i.p.) on rectal temperature and on ethanol (3 g/kg, i.p.)-induced hypothermia have been investigated in mice. Methamphetamine caused a dose-dependent hyperthermia, but methyldopa induced hypothermia, which decreased with increases in dose. Methamphetamine antagonized the hypothermic effect of ethanol, but methyldopa (1 and 2 mg/kg) did not affect it. Methyldopa (4 mg/kg), however, reversed ethanol hypothermia. Ethanol pretreatment significantly potentiated the hypothermic effect of methyldopa (4 mg/kg), and it prevented methamphetamine-induced hyperthermia. A possible central action for the tested drugs on biogenic monoamines and a peripheral component in their thermoregulatory effects are discussed in this report.
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PMID:Effects of methamphetamine and methyldopa on ethanol induced hypothermia in mice. 399 69

Tolerance to the cardioacceleratory and hypothermic effects of ethanol was studied in unanesthetized, freely-moving rats surgically implanted with EKG electrodes and biotelemetric temperature sensors. Different groups received 0.0, 1,0 or 2.0 g ethanol/kg body weight in injections given every other day for a total of nine injections. Heart rate and body temperature were recorded for 1 hr before and 2 hr after each injection. Ethanol initially induced a monophasic dose-related cardioacceleration (80 bpm) and hypothermia (1.0 degrees C) that persisted throughout the 2-hr sample period. Tolerance developed to the hypothermic, but not to the tachycardic effect of ethanol. Assuming that tolerance depends on level of impairment in specific neuronal pathways, this outcome suggests that these two effects of ethanol are not mediated through a common autonomic mechanism (e.g., vasomotor depression) and/or that tolerance to the hypothermic effect is due to alterations in pathways unique to the thermoregulatory system. Overall, the finding is consistent with those of studies showing development of tolerance to depressant, but not to excitatory drug effects.
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PMID:Dissociation of tolerance to the hypothermic and tachycardic effects of ethanol. 402 29


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