Korean J Physiol Pharmacol.
1999 Aug;3(4):383-391.
Influence of mild hypothermia on clonidine-induced cardiovascular responses in the pentobarbital-anesthetized rat
- Affiliations
-
- 1Department of Pharmacology, College of Medicine, Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul, 137-701 South Korea.
Abstract
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This study was carried out to determine whether the effects of an
alpha2-adrenoceptor agonist, clonidine, on mean arterial pressure (MAP)
and heart rate (HR) are influenced by mild hypothermia. Experiments
were performed in respiration-controlled and spontaneously breathing
pentobarbital-anesthetized rats Rectal temperature was maintained at
37.5 +/- 0.3degreeC for normothermic groups or at 35.2 +/- 0.3degreeC for
mild hypothermic groups. Intravenous injection of clonidine (1 and 2
mug/kg) produced depressor and bradycardic responses in spontaneously
breathing rats under both normothermic and mild hypothermic condition a
decrease in MAP was not altered but bradycardic response was
significantly augmented in the mild hypothermic group as compared with
the normothermic group. Under the respiration-controlled condition, the
hypotensive effect of clonidine (2 mug/kg) was reduced, whereas the
bradycardic effect was increased in mild hypothermic rats as compared
with normothermic rats. Both hypotensive and bradycardic effects of
clondine (2 mug/kg) were blocked by pretreatment with an
alpha2-adrenoceptor antagonist, yohimbine (0.5 mg/kg), in both thermal
conditions. Yohimbine (0.5 mg/kg, i.v.) alone produced signifcantly an
increase in heart rate in the mild hypothermic group than in the
normothermic group. Pretreatment with a muscarinic receptor antagonist,
atropine methylnitrate (1 mg/kg, i.v.), attenuated the bradycardic
effect of clonidine in the mild hypothermic group but not in the
normothermic group. These results suggest that clonidine-induced
bradycardia is amplified by mild hypothermia probably through an
increased parasympathetic activity.