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British Journal of Anaesthesia, Vol 82, Issue 1 74-80, Copyright © 1999 by The Board of Management and Trustees of the British Journal of Anaesthesia

LABORATORY INVESTIGATIONS

Distinct molecular sites of anaesthetic action: pentobarbital block of human brain sodium channels is alleviated by removal of fast inactivation

H. C. Wartenberg, B. W. Urban and D. S. Duch
Department of Anesthesiology and Physiology, Cornell University Medical College, 1300 York Avenue, New York, NY 10021, USA; Present address: Klinik und Poliklinik fur Anasthesiologie und spezielle Intensivmedizin, Rheinishe Friedrich-Wilhelms-Universitat Bonn, Sigmund-Freud-Stase 25, D-53105 Bonn, Germany

Fast inactivation of sodium channel function is modified by anaesthetics. Its quantitative contribution to the overall anaesthetic effect is assessed by removing the fast inactivation mechanism enzymatically. Sodium channels from human brain cortex were incorporated into planar lipid bilayers. After incorporation, channels were exposed to increasing concentrations of pentobarbital (pentobarbitone), either before or after fast inactivation had been enzymatically removed using trypsin. Anaesthetic suppression of these channels with or without the fast inactivation site was compared by analysing single channel currents. Treatment with cytoplasmic trypsin alleviated two-thirds of the pentobarbital block on open channel probability (fractional channel open time). The hyperpolarizing shift in steady-state activation caused by pentobarbital was not affected by treatment with trypsin. Extracellular trypsin was ineffective. These results support a model of general anaesthetic action on sodium channels in which anaesthetics produce a concentration-dependent shift in the distribution between activated and inactivated states towards fast inactivation. Some pentobarbital effects remained after removal of inactivation. The results support a multi-mechanistic model of anaesthetic action on brain sodium channels.
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