Low-Dose Almitrine Bismesylate Enhances Hypoxic Pulmonary Vasoconstriction in Closed-Chest Dogs

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Abstract
The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor response was studied in six closed-chest dogs anesthetized with pentobarbital and paralyzed with pancuronium. The right lung was ventilated continuously with 100% O2; the left lung was ventilated either with 100% O2 ("hyperoxia") or with an hypoxic gas mixture ("hypoxia": end-tidal oxygen tension = 60.3 .+-. 0.6 mm Hg). On two consecutive days, each dog received either almitrine (Vectarion, Servier Lab) or malic acid. Consecutive almitrine doses of 0.003, 0.03, 0.3, and 3.0 .mu.g.cntdot.kg-1.cntdot.min-1, or the equivalent volumes of malic acid without almitrine, were administered intravenously as a constant peripheral infusion for 15 min. Percent blood flow to each lung was calculated based on a variation of the traditional shunt equation. The change in percent left lung blood flow (.DELTA.% .ovrhdot.QL-VA) increased significantly between the hypoxia-no drug and the hypoxia-almitrine (3.0 .mu.g.cntdot.kg-1.cntdot.min-1) phase. No significant changes occurred during the other almitrine doses or the respective malic acid control phases. The change in arterial oxygen tension (.DELTA.PaO2) also increased significantly between the hypoxia-no drug and the hypoxia-almitrine (3.0 .mu.g.cntdot.kg-1.cntdot.min-1) phase. No significant changes occurred during the other almitrine doses or the respective malic acid control phases. It is concluded that in dogs low-dose almitrine enhances hypoxic pulmonary vasoconstriction and that this enhancement is dose-related.