The effect of isoproterenol on the development and recovery of hypoxic pulmonary hypertension. A structural and hemodynamic study.

Isoproterenol, administered intravenously during acute hypoxic exposure, is here shown to prevent about two-thirds of the rise in pulmonary artery pressure in unanesthetized male Sprague-Dawley rats with normal pulmonary vascular beds. In rats receiving continuous intravenous infusion of isoproterenol during 2 weeks' exposure to chronic hypobaric hypoxia (FiO2 0.1) the drug does not prevent either the hemodynamic or pulmonary structural changes caused by hypoxia. Similar drug administration to rats in air causes a mild increase in pulmonary artery muscularity including extension and hypertrophy of both the left and right ventricles, without changing hemodynamic findings. Isoproterenol administered during 2 weeks' recovery in air after 2 weeks' hypoxia not only prevents the usual structural recovery, but several structural features actually progress. In contrast, it does not prevent hemodynamic recovery, perhaps because the hematocrit is lower in the isoproterenol-treated rats than in rats recovering without isoproterenol. Administered in air to rats with pulmonary vascular beds remodeled by chronic hypoxia, it does not reduce pulmonary artery pressure.