Effects of sevoflurane on sympathetic neurotransmission in human omental arteries and veins

Background. Sevoflurane reduces blood pressure, the regulationof which requires an intact sympathetic neurotransmission. Thisstudy was designed to evaluate the effect of sevoflurane onthe coupling between peripheral sympathetic neurones and vascularsmooth muscle in isolated human omental vessels. Methods. Segments of arteries and veins were exposed to sevoflurane1%, 2% and 4% (corresponding to approximately 0.5, 1 and 2 MACin humans, respectively). The vessels were studied in vitroto determine the effects on (i) isometric contraction duringelectrical field stimulation (EFS) or in the presence of exogenousnorepinephrine (NE); (ii) electrical field stimulated releaseof [³H]-NE from vessel segments previously incubated with [³H]-NE;(iii) uptake of [³H]-NE. Results. In artery segments, sevoflurane 4% attenuated the contractioninduced by both EFS and exogenous NE. In vein segments, sevoflurane4% attenuated only the EFS-induced contractions. Sevoflurane1% and 2% had no effect. The release of [³H]-NE was inhibitedby sevoflurane 2% and 4% in arteries and by sevoflurane 1%,2% and 4% in veins. Sevoflurane had no effect on the uptakeof [³H]-NE in either vessel. Conclusions. Sevoflurane depresses sympathetic neuromusculartransmission in human omental vessels by reducing neuronal NErelease and NE sensitivity in arteries and by reducing NE releasein veins. This could contribute to the hypotension seen duringsevoflurane anaesthesia, at least at concentrations above 1MAC. Br J Anaesth 2003; 90: 766–73