RESUMEN
Halothane in anesthetic concentrations causes cerebral vasodilatation and decreases cerebral oxygen consumption (CMRO2). The purpose of this study was to evaluate cerebral blood flow (CBF) and CMRO2 changes associated with low concentrations of halothane. In eight normoventilated baboons with background anesthesia maintained with phencyclidine and nitrous oxide, CBF and CMRO2 were studied during the administration of end-tidal concentrations of halothane (0.125, 0.25, 0.375, 0.5, 0.75, and 1.0 vol%). Arterial blood pressure was supported by an infusion of angiotension II amide at 0.75 and 1.0 vol% of halothane to maintain an adequate cerebral perfusion pressure. In addition, cerebrovascular autoregulation was tested before and during the administration of 0.375, 0.75, and 1.0 vol% of halothane. Cerebrovascular autoregulation was assessed by observing the response of CBF to an acute increase in mean arterial pressure produced by angiotensin. CMRO2 decreased as the concentration of halothane was increased. At low halothane concentrations (0.125-0.375 vol%), CBF decreased; however, at concentrations above 0.375 vol%, CBF increased with a decrease in cerebrovascular resistance. Autoregulation was intact during 0.375 vol% of halothane, but with 0.75 and 1.0 vol% of halothane, CBF was passively dependent on cerebral perfusion pressure, suggesting impaired autoregulation.