Effects of volatile anesthetics on pulmonary vasoactivity in rats with pulmonary hypertension.

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Effects of anesthetics on vasoactivity of remodeled vessels are unknown. The purpose of this study was to investigate the effects of anesthetics on vasoactivity of pulmonary arteries from rats with monocrotaline-induced pulmonary hypertension (PH).First, electrophysiological study was performed in order to clarify the characteristics of pulmonary artery smooth muscle (PASM) cells in PH. The membrane currents in the PASM cells from PH and control rats were compared using the whole-cell patch clamp technique. The densities of Ca^<2+>-activated K^+ currents but not voltage-gated K^+ currents in PH rats were smaller than those in control rats. A depolarization of membrane potential induced by 4-AP was greater in PH than in control. Therefore, it is suggested that vasoconstriction is easily evoked in the PASM cells in PH.Then, investigation of α-adrenergic vasoconstriction was tried using pressurized pulmonary arteries in PH, however, the preparation was too difficult. In the preliminary trial with pressurized small mesenteric artery, it was found that α-agonist induced not only vasoconstriction but also endothelium-dependent oscillatory vasomotion. Because this oscillation may provide advantages in the regional control of organs, the study was extended to clarifying the mechanisms of the α-agonist-induced oscillation. The oscillation was not abolished after combined inhibition of the cyclooxygenase and NO synthase pathways. The Ca^<2+>-activated K^+ channels blockers completely abolished the remaining component of oscillation. Propofol, widely used anesthetic, potentiated the oscillation even after the combined inhibition of the cyclooxygenase and NO synthase pathways. These results suggest that theα-agonist-induced oscillation is partly mediated by EDHF, and that propofol may potentiate the EDHF-mediated hyperpolarization.