British Journal of Anaesthesia, 1995, Vol. 74, No. 5 576-582
© 1995 The Board of Management and Trustees of the British Journal of Anaesthesia
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Effect of sevoflurane on the vascular reactivity of rabbit mesenteric artery
Department of Anesthesiology, Kanagawa Dental College 82 Inaoka-Cho, Yokosuka, Kanagawa 238, Japan
Department of Pharmacology, Kanagawa Dental College 82 Inaoka-Cho, Yokosuka, Kanagawa 238, Japan
Correspondence to E.O.
Sevoflurane is well known to cause depression of cardiovascular function, but detailed information on its actions on the contractility and reactivity of blood vessels is lacking. We have assessed therefore the direct effect of this anaesthetic on the functional reactivity of isolated rabbit mesenteric artery ring preparations. We found that contractions of endothelium intact rings induced by noradrenaline and phenylephrine were significantly attenuated by 4% sevoflurane; the observation that the maximal tension generation decreased without a significant reduction in pD2 is consistent with the view that receptor dysfunction was not involved. The effect of sevoflurane was not affected by NG-monomethyl-L-arginine. Sevoflurane 4% also produced attenuation of noradrenaline-induced contractions of endothelium denuded ring preparations. The contractions of endothelium denuded ring preparations produced by noradrenaline in Ca2+-free media in the presence of K+ were not affected by 4% sevoflurane, but sevoflurane depressed external Ca2+-dependent contractions. When vasodilators (acetylcholine and nitroglycerin) were added to the bathing media in the presence of 2% sevoflurane, the endothelium dependent relaxation produced by acetylcholine, but not the endothelium-independent relaxation produced by nitroglycerin, was attenuated; superoxide dismutase inhibited the effect of sevoflurane on endothelium-dependent relaxation. These results are consistent with the view that sevoflurane inhibits 
adrenoceptor-mediated contractions of isolated rabbit mesenteric artery ring preparations; this effect may be caused by reduced Ca2+ influx, as estimated from the effect on external Ca2+ dependent contractions, but is unlikely to be caused by reduced Ca release from the sarcoplasmic reticulum of vascular smooth muscle, as estimated from noradrenaline-induced contractions in Ca2+ free bathing media. Sevoflurane may selectively attenuate endothelium-dependent relaxation by an oxygen free radical mechanism as opposed to endothelium-independent relaxation. (Br. J. Anaesth. 1995; 74: 576–582)
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