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. Fourteen baboons (Papio papio) 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 intravenously consistently reversed
hemiparesis and
hemiplegia in all baboons for as long as they lived (4 h to 8 days postocclusion).
Morphine administered intravenously converted
hemiparesis to
hemiplegia; 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 l/min higher than the highest value measured after
naloxone administration) produced no change in neurologic function. It appears that
naloxone can reverse, and
morphine exacerbate, focal ischemic
neurologic deficits produced in baboons by MCA occlusion. The observed changes in neurologic function are not associated with or mediated by alterations in core temperature or cardiopulmonary functions.