The hemodynamic effects of prostaglandin E1, sodium nitroprusside (SNP), nitroglycerin, and hydralazine were studied in a porcine model of elevated pulmonary vascular resistance (PVR) due to glass bead microembolization (60-150-μm diameter). Each animal received all four drugs. Each drug was titrated to produce a 30% reduction in mean systemic arterial pressure. Although all four drugs decreased PVR, distinct differences in the hemodynamic profiles of the four drugs were evident. Prostaglandin E1 produced the largest reduction in mean pulmonary artery pressure (from 41 ± 1 to 32 ± 9 mm Hg, mean ± SEM) and PVR (25 ± 3 to 18 ± 2 mm Hg·L-1·min-1), and did not affect the ratio of PVR to systemic vascular resistance (PVR/SVR). Sodium nitroprusside and nitroglycerin produced moderate decreases in PVR (nitroglycerin 21 ± 2 to 18 ± 2 mm Hg·L-1·min-1, SNP 22 ± 2 to 19 ± 2 mm Hg·L-1 min-1) and in mean pulmonary artery pressure (nitroglycerin 39 ± 1 to 35 ± 1; SNP 40 ± 1 to 36 ± 2 mm Hg). Both drugs significantly increased the PVR/SVR ratio. Hydralazine was the only drug that significantly increased cardiac output (1.6 ± 0.2 to 1.9 ± 0.3 L/min). Hydralazine had no significant effect on mean pulmonary artery pressure, reduced PVR to the smallest extent (11%), and resulted in the largest increase in the PVR/SVR ratio (from 0.52 ± 0.04 to 0.80 ± 0.08). In this model of increased pulmonary vasculature resistance prostaglandin E1 caused an equivalent amount of pulmonary and systemic vasodilation, as expressed by the PVR/SVR ratio. Hydralize caused the least amount of pulmonary vasodilation for a given amounts of systemic vasodilation. Nitroglycerin and SNP were intermediate in their effects between prostaglandin E1 and hydralazine.
|Original language||English (US)|
|Number of pages||7|
|Journal||Anesthesia and Analgesia|
|State||Published - Jan 1 1990|
- Embolism, pulmonary - vasodilator therapy
- Lung, embolism - vasodilator therapy