CHANGES IN NOCICEPTION, ARTERIAL BLOOD-PRESSURE AND HEART-RATE PRODUCED BY INTRAVENOUS MORPHINE IN THE CONSCIOUS RAT

The present study shows that intravenous (iv.) administration of morph ine produces dose-dependent increases in tail flick and hot plate late ncies in conscious rats. I.v. morphine also decreased heart rate, but had no significant effects on arterial blood pressure. Transection of the right vagus at the cervical level or pre-treatment with the periph erally acting opioid receptor antagonist naloxone methobromide attenua ted the increased tail flick latency produced by either 1.75 or 2.5 mg /kg morphine. In addition, either right vagotomy or naloxone methobrom ide attenuated the increased hot plate latency produced by 1.75 mg/kg of morphine but not by 2.5 mg/kg of morphine. Following pre-treatment with naloxone methobromide, 1.75 and 2.5 mg/kg of morphine produced a small pressor response 1-3 min after injection. The bradycardia produc ed by 1.75 mg/kg of morphine was attenuated by naloxone methobromide, but not by right vagotomy. The bradycardia produced by 2.5 mg/kg of mo rphine was attenuated by either naloxone methobromide or vagotomy. The se data obtained in the conscious rat are similar to previous reports using pentobarbital-anesthetized rats except for the following: (i) th e dose-response function for inhibition of the tail flick was shifted to the right in conscious rats, (ii) the depressor response to morphin e observed in anesthetized rats was attenuated in conscious rats, (iii ) following naloxone methobromide, but not unilateral vagotomy, i.v. m orphine produced a pressor response in the conscious rat, and (iv) uni lateral vagotomy was not as effective in attenuating the antinocicepti on and bradycardia in conscious rats as bilateral vagotomy is in pento barbital-anesthetized rats.