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ANESTHETIC PHARMACOLOGY

The Differential Effects of Halothane and Isoflurane on Electroencephalographic Responses to Electrical Microstimulation of the Reticular Formation

Department of Anesthesiology and Pain Medicine, Section of Neurobiology, Physiology and Behavior, University of California, Davis, Davis, California

Address correspondence and reprint requests to Joseph F. Antognini, MD, Department of Anesthesiology TB-170, University of California, Davis, Davis, CA 95616. Address e-mail to jfantognini{at}ucdavis.edu.

Isoflurane and halothane cause electroencephalographic (EEG) depression and neuronal depression in the reticular formation, a site critical to consciousness. We hypothesized that isoflurane, more than halothane, would depress EEG activation elicited by electrical microstimulation of the reticular formation. Rats were anesthetized with either halothane or isoflurane and stimulating electrodes were positioned in the reticular formation. In a crossover design, anesthetic concentration was adjusted to 0.8 and 1.2 minimum alveolar concentration (MAC) of halothane or isoflurane and electrical microstimulation was performed and the EEG responses were recorded. Microstimulation increased the spectral edge and median edge frequencies 2–2.5 Hz at 0.8 MAC for halothane and isoflurane and 1.2 MAC halothane. At 1.2 MAC isoflurane, burst suppression occurred and microstimulation decreased the period of isoelectricity (24% ± 19% to 8% ± 7%; P < 0.05), whereas the spectral edge and median edge frequencies were unchanged. At anesthetic concentrations required to produce immobility, the cortex remains responsive to electrical microstimulation of the reticular formation, although the EEG response is depressed in the transition from 0.8 to 1.2 MAC. These data indicate that cortical neurons remain responsive to synaptic input during isoflurane and halothane anesthesia.

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