Effects of ethanol on thermoregulation.
Clinical reports of accidental hypothermia in alcohol intoxicated individuals exposed to low ambient temperature ( Paton , 1983) have generally been borne out by experimental studies in healthy volunteers. Small doses of ethanol, given to human subjects at normal ambient temperature (Ta), have very little effect on body temperature but a combination of large dose, low Ta and vasodilatation provoked by strenuous exercise, causes a sharp fall in rectal temperature. In experimental animals, the use of relatively larger doses of alcohol and more extreme temperatures, both above and below the thermoneutral zone, has shown that the effect of ethanol is essentially poikilothermic, i.e. an impairment of adaptation to both heat and cold. This effect has been studied in greater detail, in relation to each of the basic thermoregulatory processes. Though small doses of alcohol may increase the metabolic rate under some circumstances, the most common effect at low Ta is inhibition of shivering and therefore reduction of thermogenesis. At the same time it tends to cause increased heat loss by cutaneous vasodilatation. This makes for a greater feeling of comfort in the cold exposed subjects but increases in rate of fall of core temperature. The combination of decreased thermogenesis and increased heat loss, despite falling body temperature, is suggestive of a lowering of the set-point of the thermoregulatory control mechanisms. Consistent with this is a slight increase in ventilatory heat loss after low doses of ethanol but larger doses cause respiratory depression, so that heat loss through the lungs is minor. However, at high Ta ethanol caused hyperthermia in experimental animals and shows enhanced lethality, so that impairment of thermoregulatory effector mechanisms seems to be at least as important as change in set-point. Studies of the effects of ethanol on electrophysiological activity of single neurons in the pre-optic area and anterior hypothalamus (POAH), biochemical activities of neuronal membranes, hypothalamic blood flow, conventional neurotransmitters, amino acid putative neurotransmitters, neuropeptides, prostaglandins and inorganic ions have all failed so far to yield a clear comprehensive picture of the mechanisms by which ethanol affects thermoregulation. In each case, contradictory evidence has been obtained concerning the consequences of ethanol administration, whether by oral, intraperitoneal, intravenous, intracerebroventricular, or direct local (POAH) route.(ABSTRACT TRUNCATED AT 400 WORDS)
D000437:Alcoholism / Q000503:physiopathology; D000818:Animals; D001519:Behavior / Q000502:physiology; D001833:Body Temperature Regulation / Q000187:drug effects*; D002746:Chlorpromazine / Q000494:pharmacology; D003080:Cold Temperature; D004347:Drug Interactions; D004361:Drug Tolerance; D004594:Electrophysiology; D000431:Ethanol / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects; D006358:Hot Temperature; D006801:Humans; D006830:Hydralazine / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology; D009294:Narcotics / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D012119:Respiration / Q000187:drug effects; D013045:Species Specificity; D013696:Temperature
D009294:Narcotics; D009419:Nerve Tissue Proteins; D018377:Neurotransmitter Agents; D011453:Prostaglandins; D006830:Hydralazine; D000431:Ethanol; D002746:Chlorpromazine