Prostaglandins and fetal cardiac output distribution in the lamb.

With the use of a triple thermodilution technique in 17 fetal lambs, combined with microsphere estimations in 7, the effects of indomethacin prostaglandin (PG) I2 and PGE2 on cardiac output and its distribution were measured. Indomethacin (0.2 mg/kg) induced a main pulmonary artery-to-aorta pressure gradient, which peaked within 45-60 min and persisted for 2-3 h. PGE2 abolished this gradient (threshold 50 ng X kg-1 X min-1), while PGI2 in doses up to 100 ng X kg-1 X min-1 increased it. Indomethacin did not change total cardiac output but altered its distribution (right ventricular output, left ventricular output) and increased the percentage of right ventricular output flowing to the lungs. Ductal flow decreased concomitantly. After indomethacin, PGI2 further decreased ductal flow, increased pulmonary flow, and decreased pulmonary vascular resistance. PGE2 restored the original right ventricular-to-total cardiac output ratio, although ductus flow did not return to base-line levels. Pulmonary resistance increased slightly, reflecting decreased pulmonary flow, associated with decreased right ventricular output. Thus PGE2 was more effective on the ductus than on the pulmonary circulation. PGI2 did not relax the ductus but was a potent pulmonary vasodilator. Neither PGI2 nor PGE2 nor indomethacin changed total cardiac output but all altered its distribution.