• K Thorlacius, C Zhoujun, and M Bodelsson.
• Department of Anaesthesiology and Intensive Care, University Hospital, SE-221 85 Lund, Sweden.
• Br J Anaesth. 2003 Jun 1; 90 (6): 766-73.

BackgroundSevoflurane reduces blood pressure, the regulation of which requires an intact sympathetic neurotransmission. This study was designed to evaluate the effect of sevoflurane on the coupling between peripheral sympathetic neurones and vascular smooth muscle in isolated human omental vessels.MethodsSegments of arteries and veins were exposed to sevoflurane 1%, 2% and 4% (corresponding to approximately 0.5, 1 and 2 MAC in humans, respectively). The vessels were studied in vitro to determine the effects on (i) isometric contraction during electrical field stimulation (EFS) or in the presence of exogenous norepinephrine (NE); (ii) electrical field stimulated release of [(3)H]-NE from vessel segments previously incubated with [(3)H]-NE; (iii) uptake of [(3)H]-NE.ResultsIn artery segments, sevoflurane 4% attenuated the contraction induced by both EFS and exogenous NE. In vein segments, sevoflurane 4% attenuated only the EFS-induced contractions. Sevoflurane 1% and 2% had no effect. The release of [(3)H]-NE was inhibited by sevoflurane 2% and 4% in arteries and by sevoflurane 1%, 2% and 4% in veins. Sevoflurane had no effect on the uptake of [(3)H]-NE in either vessel.ConclusionsSevoflurane depresses sympathetic neuromuscular transmission in human omental vessels by reducing neuronal NE release and NE sensitivity in arteries and by reducing NE release in veins. This could contribute to the hypotension seen during sevoflurane anaesthesia, at least at concentrations above 1 MAC.

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