The ductus arteriosus is a shunt blood vessel of fetal life; it extends between the pulmonary artery and the aorta. It shunts deoxygenated blood from the main pulmonary artery to the descending aorta. Over half of the blood flow in the descending aorta is diverted to the umbilico-placental circulation (Heymann and Rudolph, 1975), where gaseous exchange takes place. The timing of closure of the ductus after birth varies between species (Heymann and Rudolph, 1975), but it is usually complete within 48 h in humans (Drayton and Skidmore, 1987). Ductal patency in utero is an active state principally maintained by the potent dilator effect of prostaglandins (PGs) b (Coceani and Olley, 1988). Closure at birth is because of contraction of its smooth muscle. This is secondary to withdrawal of dilation and active stimulation of contraction, particularly by increased oxygen tension (Coceani and Olley, 1988). The control of the ductus is clinically important in a number of areas. Contraction of the ductus, with or without fetal heart failure, is a recognized side effect of administration of prostaglandin H synthase (PGHS) inhibitors to the mother (Van den Veyver and Moise, 1993). Failure of ductal closure after birth is a common complication of premature delivery, and, conversely, in some forms of congenital heart disease, survival of the neonate is dependent on persistent patency of the ductus (see Gersony, 1986 for review). Understanding the role of PGs in the control of the ductus led directly to therapies in the human neonate, specifically, indomethacin to close the ductus and E series PGs to maintain its patency.

This review seeks to summarize the current state of knowledge of the factors that maintain ductal patency in utero and promote ductal contraction after birth. It also seeks to identify potential novel therapeutic strategies for avoiding ductal contraction as a side effect of maternal anti-PG therapy and for the safer and more effective manipulation of ductal patency in the human neonate.