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

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.

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.

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.

Our results suggest that desflurane may have a local vasoconstrictive effect independent of endothelium and NO synthase activity. The mechanism remains to be determined.