Dissociation of tolerance to the hypothermic and tachycardic effects of ethanol.
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.
D000818:Animals; D001831:Body Temperature / Q000187:drug effects*; D004361:Drug Tolerance; D004566:Electrodes; D000431:Ethanol / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects*; D008297:Male; D051381:Rats; D013686:Telemetry
D000431:Ethanol