Desflurane, compared to halothane, augments phenylephrine-induced contraction in isolated rat aorta smooth muscle

Purpose: The mechanism responsible for the mediation of hypertension in res ponse to increased desflurane levels is unclear. This study compared the ef fect of desflurane and halothane on phenylephrine (PE)-induced contraction in rat aorta ring and the effect of desflurane in the presence and absence of nitric oxide (NO) synthase activity Methods: Endothelium-free rat aorta rings were exposed serially to 10(-7)M. 10(-6)M and 10(-5)M PE alone and subsequently in the presence of 2 MAC des flurane and halothane. Secondly, endothelium-free preparations were exposed to 10(-6)M PE serially in the presence of 0, 1, 2 and 3 MAC desflurane and halothane. Thirdly using an endothelium-intact preparation, the effect of desflurane on PE-induced contraction was examined, in the presence or absen ce of NG-nitro-L-arginine (L-NNA), an inhibitor of constitutive and inducib le NO synthase. Results: Contraction amplitudes secondary to 10(-6) and 10(-5)M PE in endot helium-free preparations were increased by 74% and 36% respectively (P (0.0 5) in the presence of 2 MAC desflurane compared to controls, in endothelium - free preparations. contraction amplitudes secondary to 10(-6)M PE were in creased in the presence of I and 2 MAC desflurane by 32% and 18% respective ly (P <0.05) and reduced by 16% in the presence of 3 MAC halothane (P <0.05 ), In endothelium-intact preparations an expected absolute increase in cont raction amplitude occurred in the presence of L-NNA but the desflurane effe ct was detectable both in the presence and absence of L-NNA. Conclusion: Our results suggest that desflurane may have a local vasoconstr ictive effect independent of endothelium and NO synthase activity The mecha nism remains to be determined.