Hemodynamic profiles of prostaglandin E1, isoproterenol, prostacyclin, and nifedipine in experimental porcine pulmonary hypertension
- 1 January 1991
- journal article
- laboratory investigation
- Published by Wolters Kluwer Health in Critical Care Medicine
- Vol. 19 (1) , 60-67
- https://doi.org/10.1097/00003246-199101000-00016
Abstract
Background and Methods We compared the hemodynamic effects of four vasodilators in experimental embolic pulmonary hypertension in a randomized controlled trial, using nine pigs weighing 16 to 23 kg. After anesthesia induction and cannulation with arterial, central venous, and thermodilution output pulmonary artery catheters, animals were repetitively embolized with glass beads (60 to 160 μ) in order to establish pulmonary hypertension (pulmonary artery pressure [PAP] doubled from baseline). Prostaglandin E1 (PGE1), isoproterenol, prostacyclin (PGI2), and nifedipine were compared at doses producing equivalent reduction in systemic BP. Results Only PGE1 and PGI2 decreased both PAP and pulmonary vascular resistance (PVR). PGE1 decreased PAP from 39 ± 1 to 33 ± 1 mm Hg; prostacyclin decreased PAP from 38 ± 1 to 31 ± 1 mm Hg and produced the largest increase in cardiac output (Qt). Isoproterenol did not change PAP, markedly increased heart rate (162 ± 8 to 216 ± 11 beats/min), and resulted in significant arrhythmias. Nifedipine increased PVR from 1044 ± 113 to 1125 ± 100 dynesec·cm-5 and decreased Qt. Conclusion Vasodilators demonstrate unique hemodynamic drug profiles. Isoproterenol infusion is characterized by tachycardia and arrhythmias. Both PGE1 and PGI2 effectively decrease PAP and PVR. Nifedipine depressed Qt significantly in this glass-bead embolization model of acute pulmonary hypertension. (Crit Care 1991; 19:60)Keywords
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