NALOXONE REVERSAL AND MORPHINE EXACERBATION OF NEUROLOGIC DEFICITS SECONDARY TO FOCAL CEREBRAL-ISCHEMIA IN BABOONS

The effects of an opiate agonist (morphine) and antagonist (naloxone) on neurologic function in conditions of acute and subacute focal cerebral ischemia were tested in a baboon model. Baboons (P. papio) (14) underwent unilateral transorbital microsurgical occlusion of the middle cerebral artery (MCA). Blood pressure, heart rate and core temperature were monitored continuously; frequent arterial blood gas measurements were made. Cardiac output, cardiac filling pressures and regional cerebral blood cross-flow were measured in selected baboons. Naloxone administered i.v. consistently reversed hemiparesis and hemiplegia in all baboons for as long as they lived (4 h to 8 days postocclusion). Morphine administered i.v. converted hemiparesis to hemiplesia; this effect was naloxone-reversible. There were no significant changes in any parameter measured after the administration of either drug. Phenylephrine (used to elevate mean arterial pressure to 20 mm higher than the highest pressure measured after naloxone administration) and isoproterenol (used to elevate cardiac output to 1 1/min higher than the highest value measured after naloxone administration) produced no change in neurologic function. Naloxone can reverse, and morphine exacerbate, focal ischemic neurologic deficits produced in baboons by MCA occlusion. The changes in neurologic function are not associated with or mediated by alterations in core temperature or cardiopulmonary functions.