Cerebral and systemic vascular effects of naloxone in pentobarbital-anesthetized normal dogs

Turner, D.M.; Kassell, N.F.; Sasaki, T.; Comair, Y.G.; Beck, D.O.; Klein, S.L.

Neurosurgery 14(3): 276-282


ISSN/ISBN: 0148-396X
PMID: 6709151
DOI: 10.1227/00006123-198403000-00003
Accession: 042482844

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In this study, 10 mongrel dogs were anesthetized with sodium pentobarbital and nitrous oxide. Blood flow was determined using the radioactive microsphere technique before and after the bolus intravenous injection of naloxone (10 mg/kg). Naloxone significantly increased cerebral blood flow to cerebral cortex and the total cerebral hemisphere without an associated change in the cerebral metabolic rate of oxygen. The increase in cerebral blood flow was proportional to the elevation in mean arterial pressure. There were no consistent changes in electrical activity as measured by electroencephalography (EEG) and Fourier analysis of EEG. Systemically, naloxone induced a proportional rise in mean arterial pressure and peripheral vascular resistance and also stimulated the myocardium, as evidenced by an improved cardiac index and stroke volume. These data suggest that naloxone may interfere with cerebral autoregulation or have direct vasodilatory effects on cerebral blood vessels that are not associated with opiate receptor blockade or changes in cerebral metabolism. In addition, naloxone did not appear to reverse the cerebral depressive effects of pentobarbital. Systemically, naloxone seemed to potentiate pentobarbital-induced vasoconstriction and reverse myocardial depression.