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 dyne·sec·cm-5 and decreased Qt. Conclusions: 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.
- Blood pressure
- Calcium-channel antagonists
- Lung, shunting, vasodilators
- Prostaglandin E, prostacyclin
- Pulmonary hypertension