ISCHEMIC DEPOLARIZATION DURING HALOTHANE-NITROUS OXIDE AND ISOFLURANE-NITROUS OXIDE ANESTHESIA - AN EXAMINATION OF CEREBRAL BLOOD-FLOW THRESHOLDS AND TIMES TO DEPOLARIZATION

Background: Isoflurane-N2O anesthesia (as compared with halothane-N2O) reduces the cerebral blood flow (CBF) at which electroencephalographi c changes occur in humans subjected to carotid occlusion. In contrast, no differences were seen in rats when cortical depolarization (instea d of the electroencephalogram) was used as the ischemic marker during equi-MAC isoflurane-N2O and halothane-N2O anesthesia. To extend these findings, we used laser-Doppler flowmetry to continuously examine CBF (CBFLDF) and attempted to better define the relation between CBF and t he time to depolarization (as a measure of the rate of energy depletio n after ischemia). Methods: Cortical CBFLDF was measured in normotherm ic, normocarbic rats, and the cortical direct-current potential was re corded using glass microelectrodes. Animals were anesthetized with 0.7 5 MAC halothane or 0.75 MAC isoflurane, both in 60% N2O. After baselin e recordings, both carotid arteries were occluded. Five minutes later mean arterial pressure was rapidly reduced to and held at target value s of 50, 45, 40, 30 or 0 mmHg. This mean arterial pressure was maintai ned (and CBFLDF was continually monitored) until depolarization occurr ed, or for a maximum of 20 min. Results: CBFLDF values before and afte r carotid occlusion (but before hypotension) were similar in the two g roups. As intended, CBFLDF decreased as postocclusion mean arterial pr essure was reduced and the incidence of cortical depolarization increa sed. The delay until depolarization, defined as the interval between t he moment CBFLDF reached 25% of the preocelusion baseline until depola rization occurred, decreased as CBFLDF was reduced. However, there wer e no intergroup differences except after a circulatory arrest (CBF = 0 ), where cortical depolarization was seen approximate to 30 s later in isoflurane-N2O-anesthetized rats. Conclusions: The CBF threshold for cortical depolarization as measured by laser-Doppler flowmetry did not differ significantly between halothane-N2O- and isonurane-N2O-anesthe tized rats. There were also no important differences in the times unti l depolarization, other than a small difference when flow = 0. If the time to depolarization is reflects the potential ischemic injury, the it is unlikely that isoflurane-N2O conveys any protective advantage re lative to halothane-N2O.