TY - JOUR
T1 - Dissociation of tolerance to the hypothermic and tachycardic effects of ethanol
AU - Peris, Joanna
AU - Cunningham, Christopher L.
N1 - Funding Information:
This research was supported in part by a training grant from the National Heart Lung and Blood Institute (HL07332) and by research grants from the Medical Research Foundation of Oregon and the National Institute on Alcohol Abuse and Alcoholism (AA06161). John Crabbe is thanked for his comments on an earlier version of the manuscript.
PY - 1985/6
Y1 - 1985/6
N2 - 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°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 effects 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.
AB - 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°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 effects 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.
KW - Body temperature
KW - Ethanol
KW - Heart rate
KW - Rats
KW - Tolerance
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U2 - 10.1016/0091-3057(85)90305-3
DO - 10.1016/0091-3057(85)90305-3
M3 - Article
C2 - 4023029
AN - SCOPUS:0021874784
SN - 0091-3057
VL - 22
SP - 973
EP - 978
JO - Pharmacology, Biochemistry and Behavior
JF - Pharmacology, Biochemistry and Behavior
IS - 6
ER -