Influence of Mild Hypothermia on Clonidine-Induced Cardiovascular Responses in the Pentobarbital-Anesthetized Rat

Influence of Mild Hypothermia on Clonidine-Induced Cardiovascular Responses in the Pentobarbital-Anesthetized Rat

<P> This study was carried out to determine whether the effects of an α<SUB>2</SUB>-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&#8273;0.3<SUP>o</SUP>C for normothermic groups or at 35.2&#8273;0.3<SUP>o</SUP>C for mild hypothermic groups. Intravenous injection of clonidine (1 and 2 μg/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 μg/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 μg/kg) were blocked by pretreatment with an α<SUB>2</SUB>-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.