Endogenous opioids are released in great amounts in perinatal asphyxia. The role of this release has been unclear. In a study of cerebral blood flow and oxygen metabolism in 5 hypoxic newborn lambs, naloxone blocking of opioid receptors resulted in a proportional increase in telencephalic cerebral blood flow and oxygen metabolism. It is suggested that endogenous opioid release protects the neonatal brain in hypoxia by diminishing the cerebral metabolic rate of oxygen.

SummaryResuscitation of the brain following total circulatory arrest may be impeded by difficulty in establishing cerebral tissue perfusion, a post-ischemic “low-flow” state. We have confirmed this hypothesis in a rat model of total cerebral ischemia and have demonstrated marked improvement in post-ischemic brain tissue perfusion following epinephrine injection. This is mainly due to the systemic vascular effects of epinephrine, resulting in improved central aortic pressure and cerebral perfusion pressure. Hyperkalemic induced vasoconstriction has also been postulated as a cause of the “low-flow”. We have, therefore, investigated the in vitro effects of increasing potassium ion concentration on cerebrovascular smooth muscle strips. Large arteries constrict, while small arteries dilate in response to hyperkalemia. The net effect on cerebral blood flow remains unsettled. Our research to date suggests that resuscitation of the totally ischemic brain, in animal models at least, is enhanced by epinephrine, mainly via its effects on central aortic pressure.

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