title: Mechanisms of the "low-flow" state during resuscitation of the totally ischemic brain.
abstract: Resuscitation of the brain following total circulatory arrest may be impeded by difficulty in establishing cerebral tissue perfusion, a postischemic "low-flow"state. We have confirmed this hypothesis in a rat model of total cerebral ischemia and have demonstrated marked imporvement in post-ischemic brain tissue perfusion following epinephrine injection. This is mainly due to the systemic vascular effects of epinephrine, resulting in improved central arotic 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.
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply*; D002417:Cattle; D002536:Cerebral Arteries / Q000187:drug effects; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004837:Epinephrine / Q000494:pharmacology*; D006323:Heart Arrest / Q000503:physiopathology*; D066298:In Vitro Techniques; D007511:Ischemia / Q000503:physiopathology*; D009130:Muscle, Smooth / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012151:Resuscitation / Q000379:methods*
chemical_list: D011188:Potassium; D004837:Epinephrine