The present study shows that intravenous (i.v.) administration of
morphine produces dose-dependent increases in tail flick and hot plate latencies 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 peripherally acting
opioid receptor antagonist naloxone methobromide attenuated the increased tail flick latency produced by either 1.75 or 2.5 mg/kg
morphine. In addition, either right
vagotomy or
naloxone methobromide 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 produced 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
morphine was attenuated by either
naloxone methobromide or
vagotomy. These data obtained in the conscious rat are similar to previous reports using
pentobarbital-anesthetized rats except for the following: (i) the dose-response function for inhibition of the tail flick was shifted to the right in conscious rats, (ii) the depressor response to
morphine observed in anesthetized rats was attenuated in conscious rats, (iii) following
naloxone methobromide, but not unilateral
vagotomy, i.v.
morphine produced a pressor response in the conscious rat, and (iv) unilateral
vagotomy was not as effective in attenuating the antinociception and
bradycardia in conscious rats as bilateral
vagotomy is in
pentobarbital-anesthetized rats.