PROSTAGLANDIN E-1 (PGE-1) & PULMONARY VASCULAR RESIS- TANCE IN NEONATAL LAMBS

Abstract

PGE-1, a known pulmonary vasodilator in isolated lungs, has been proposed as a mediator of the rapid fall in pulmonary vascular resistance (PVR) in neonates. A previous study found that in fetal animals a 50% drop in PVR was accompained by severe systemic effects including a 44% drop in placental flow. To exclude such effects we studied chronic PGE-1 infusion directly into the pulmonary circulation of 7 neonatal lambs. Animals were instrumented in utero under maternal anesthesia. Peripheral arterial and venous catheters were placed. Thoracotomy was performed with placement of a pulmonary arterial catheter and a pulmonary trunk electromagnetic flow transducer. The ductus was ligated, the animal delivered, and mechanical ventilation instituted. Systemic and pulmonary arterial pressures, pulmonary arterial flows, heart rate, and arterial blood gases were monitored. PVR was calculated before and during infusion under normoxemic and hypoxemic conditions. In 9 infusions in 7 animals, basal PVR was 0.225 mm/Hg/ml/min and rose to 0.521 with hypoxia. Basal systemic vascular resistance (SVR) was 0.534, and rose to 0.568 with hypoxia. With PGE-1 infusion at a mean dose of 1.6 mcg/kg/min PVR fell 27% to 0.185 in room air while SVR fell 25% to 0.400. Under hypoxic conditions PVR fell 49% to 0.264 while SVR fell 44% to 0.319. We conclude that PGE-1 is a nonspecific vasodilator which during infusion is not degraded in a single pass through the lungs. It decreases PVR and SVR equally during both normoxemia and hypoxemia.