American Journal of Physiology-Heart and Circulatory Physiology · 1977 · 42 citations · 0 references
MedicineAnesthesiologyNeurosurgeryAnesthesiaGeneral AnesthesiaNeuroanesthesiologyAnesthesia For NeurosurgeryCerebral Blood FlowCerebral Perfusion MonitoringCerebrovascular PhysiologyHemodynamic Response To AnesthesiaAnaesthetic Effects On Cerebral PhysiologyAnesthetic Effects On Cerebral Blood FlowBlood FlowCerebral Blood Flow AlterationsCerebral Blood Flow EffectsHalothane AnesthesiaHemodynamic Effects Of AnesthesiaPhysiologic Effects Of Anesthesia
Past studies suggest that halothane causes cerebrovascular dilatation and increased cerebral blood flow (CBF); these properties may be relevant to its use for neurosurgical procedures. We studied CBF autoregulation in monkeys during anesthesia with 66% N2O/33% O2 and with 0.5%, 1.0%, and 2.0% inspired halothane at various cerebral perfusion pressures (CPP) achieved by infusion of trimethaphan camsylate or phenylephrine. CBF was measured by monitoring brain xenon-133 clearance after intra-arterial injection of the isotope in saline. CBF autoregulation was intact during N2O/O2 and during 0.5% halothane/N2O/O2 anesthesia at CPPs ranging from 50 to 100 mmHg, but began to fail at 1.0% halothane. Complete loss of autoregulation occurred during 2% halothane/N2O/O2 anesthesia. Estimated brain O2 consumption fell by 30%, 40%, and 50% during 0.5%, 1.0%, and 2.0% halothane anesthesia, respectively, compared to O2 consumption during N2O/O2 anesthesia (100%).