Studies of nuclear magnetic resonance imaging and regional cerebral glucose metabolism in acute cerebral ischemia: possible mechanism of opiate antagonist therapeutic activity.
Using unilateral carotid artery ligation in the gerbil as a model of cerebral ischemia, both nuclear magnetic resonance (NMR) imaging and a newly developed double-label autoradiographic technique have been employed to investigate the physiologic mechanism of opiate action during cerebral ischemia. While several parameters of the NMR image have been demonstrated to reflect focal cerebral ischemic lesions, neither 2 mg/kg naloxone nor 10 mg/kg morphine sulfate had an effect on any of the parameters of the NMR image at any time point during the 24 hr experiment. While no consistent changes could be measured in the metabolic rate immediately about the ischemic region, results from double-label 2-deoxyglucose autoradiographic studies indicate that there are marked focal increases in metabolic rate in several subcortical nuclei bilaterally following the administration of naloxone. While no significant change was noted in the thalamus or arcuate nucleus, naloxone produced a significant elevation in glucose metabolic rate in the substantia nigra, periaqueductal grey and the red nucleus. The significance of these effects are discussed and a mechanism for the beneficial effect of opiate antagonists on neurologic deficit following ischemic cerebral lesions is proposed.
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D005849:Gerbillinae; D005947:Glucose / Q000378:metabolism*; D007700:Kinetics; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D009270:Naloxone / Q000494:pharmacology*
D009270:Naloxone; D005947:Glucose