147 PATENT DUCTUS ARTERIOSUS: BIOCHEMICAL STUDIES

Abstract

Whether patency or constriction of the ductus arteriosus is related more importantly to alterations in circulating levels of prostaglandins (PG's) or with alterations in PG synthetase activity within the ductus itself is conjectural. In the present study the latter possibility was examined by evaluating the ability of the ductus arteriosus and other fetal vascular tissues to synthesize from intermediate endoperoxide (PGH2) various terminal prostaglandins. Fetal lamb ductus arteriosus generated only the potent vasodilator PGI2. The aorta and pulmonary artery produced twice the PGI2 of ductus arteriosus while vena cava produced half as much. None of these vessels produced the potent vasoconstrictor, thromboxane A2 (TXA2). In contrast, adult lung, but not fetal lung, produced abundant quantities of TXA2. Thus, ductus arteriosus may be more profoundly affected by PG synthetase inhibition (used clinically in premature infants) than other arteries. Moreover, an interplay is suggested between lung-derived TXA2 and PGI2 production within the wall of the ductus per se that promotes ductal constriction. The altered circulatory pathways associated with birth foster constriction of the ductus by providing a change in the interaction between the potent vasoactive PG's. The data suggest an explanation for prolonged ductal patency in the face of lung immaturity, for the normal process of ductal closure, and for the ability clinically to manipulate PG metabolism to alter ductal caliber.

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