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

摘要

PURPOSE: The mechanism responsible for the mediation of hypertension in response to increased desflurane levels is unclear. This study compared the effect 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 desflurane 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 absence of NG-nitro-L-arginine (L-NNA), an inhibitor of constitutive and inducible NO synthase. RESULTS: Contraction amplitudes secondary to 10(-6) and 10(-5) M PE in endothelium-free preparations were increased by 74% and 36% respectively (P <0.05) in the presence of 2 MAC desflurane compared to controls. In endothelium-free preparations, contraction amplitudes secondary to 10(-6) M PE were increased in the presence of 1 and 2 MAC desflurane by 32% and 18% respectively (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 contraction amplitude occurred in the presence of L-NNA but the desflurane effect was detectable both in the presence and absence of L-NNA. CONCLUSION: Our results suggest that desflurane may have a local vasoconstrictive effect independent of endothelium and NO synthase activity. The mechanism remains to be determined.