• Joseph F Antognini, Richard Atherley, and Earl Carstens.
• Department of Anesthesiology and Pain Medicine, University of California-Davis, Davis, CA 95616, USA. jfantognini@ucdavis.edu
• Anesth. Analg. 2003 Apr 1;96(4):999-1003, table of contents.

UnlabelledAnesthetics act in the spinal cord to ablate both movement and the ascending transmission of nociceptive information. We investigated whether a spinal cord action of isoflurane affected cortical activity as determined by the electroencephalogram desynchronization that occurs after electrical stimulation of the midbrain reticular formation (MRF). Six goats were anesthetized with isoflurane, and neck dissections were performed to permit differential isoflurane delivery to the head and torso. The electroencephalogram was recorded before, during, and after focal electrical stimulation (0.05, 0.1, 0.2, 0.3, and 0.4 mA) in the MRF; in each animal, the brain isoflurane was maintained constant ( approximately 1%). When the torso isoflurane was 0.3% +/- 0.1%, the spectral edge frequency after MRF electrical stimulation (15.3 +/- 1.7 Hz, averaged across all stimulus currents) was more than the spectral edge frequency when the torso isoflurane was 1.2% +/- 0.2% (12.9 +/- 1.0 Hz, averaged across all stimulus currents; P < 0.05). Bispectral index values were similarly affected: 60 +/- 6 when torso isoflurane was low versus 53 +/- 7 at high torso isoflurane (P < 0.05). These results suggest that a spinal depressant action of isoflurane on ascending somatosensory transmission can modulate reticulo-thalamocortical arousal mechanisms, hence possibly reducing anesthetic requirements for unconsciousness and amnesia.ImplicationsIsoflurane action in the spinal cord indirectly reduces the cortical activity associated with electrical stimulation of the reticular formation, an effect that might contribute to anesthetic-induced amnesia and unconsciousness.

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