139 PLASMA PROSTAGLANDIN E AND F₂a IN PREMATURE INFANTS WITH PATENT DUCTUS ARTERIOSIS

Abstract

The aim of the project was to determine the relation between the level of PGE and PGF₂α and the presence or absence of PDA in premature infants. In infants with clinical PDA, ages 1-26 days, the PGE and PGF₂α were 1443.10±153.78 and 766.50±70.60pg/ml, respectively;statistically insignificant from cord levels of term infants previously obtained in this laboratory. After improvement of the ductal shunt, PGE significantly decreased (p < 0.01) to 297.57±60.14 and PGF₂α (p < 0.01) to 164.66±54.53pg/ml. This decrease occurred spontaneously, with Indocin^R administration or by surgical ligation, and is comparable to levels in term infants at 3 days of age without evidence of ductal shunts. Representative examples follow:

Since catabolism of prostaglandins occurs in the lung with the majority being removed in a single pass, the high PG levels in premature infants with PDA may be due to continuation of in utero shunting of blood away from the lung and/or decreased catabolism. The decrease in PG levels with the decreased ductal shunt may be secondary to improved lung perfusion. These data suggest the patency of the ductus arteriosus may be the etiology of the elevated PG levels and not result from the elevated levels.

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