Comparative studies on the hemodynamic effects of prostaglandin E1 prostacyclin, and tolazoline upon elevated pulmonary vascular resistance in neonatal swine

Forty-eight hour old anesthetised and ventilated neonatal piglets were cannulated in order to measure pressures, blood gases and cardiac outputs (CO) from which pulmonary (PVR) and systemic (SVR) vascular resistances were calculated. After baseline measurements had been made inspired gases were altered to produce hypoxemia and hypercapnia, to raise PVR. Animals then received Prostaglandin E₁ (PGE₁), Tolazoline (TOL), and Prostacyclin (PGI₂) in varying dosages until PVR was reduced or the dosage no longer tolerated.

With “hypoxia” CO, PVR and pulmonary artery (PA) pressures rose; aortic pressure also rose although SVR tended to fall. PGE₁ (5μg/kg/min) and PGI₂ (1.0 μg/kg/min) both produced a significant fall in PVR. The decrease in PVR with TOL (1 mg/kg/10 minutes and 2 mg/kg/l hour) was less consistent and in surviving animals did not achieve statistical significance by multivariate analysis. SVR fell with all drugs although the change with TOL was again non-significant. With both PGI₂ and TOL there was a trend for CO to rise and, although this did not reach significant levels, it restricted the drop in arterial pressure to approximately control levels. The fall in arterial pressure with PGE₁ was greater. The death rate with treatment with TOL was much higher than that seen with the other two drugs.

Circulatory changes in a group of animals with normal blood gases treated with PGI₂ (1 μg/kg/min) were similar to those seen with the hypoxic group.

In this preparation PGI₂ appeared the most satisfactory drug for the treatment of elevated PVR.