11 Locally produced and circulating PGE 2 and PGI 2 in the fetus cause vasodilation of the ductus arteriosus via interaction with ductal prostanoid receptors, 12 and circulating PGE 2 and PGI 2 levels are high in the fetus because of production by the placenta and decreased metabolism in the fetal lungs.Īfter birth, the abrupt increase in oxygen tension inhibits ductal smooth muscle voltage-dependent potassium channels, which results in an influx of calcium and ductal constriction. The intima of the ductus arteriosus is thickened and irregular, with abundant mucoid material, sometimes referred to as intimal cushions.įetal patency of the ductus arteriosus is controlled by many factors, the most important of which are relatively low fetal oxygen tension 10 and cyclooxygenase-mediated products of arachidonic acid metabolism (primarily prostaglandin and prostacyclin ). 4–9 Whereas the mediae of surrounding aorta and pulmonary artery are composed mainly of circumferentially arranged layers of elastic fibers, the media of the ductus arteriosus is composed of longitudinally and spirally arranged layers of smooth muscle fibers within loose, concentric layers of elastic tissue. Grossly, the constitution of the fetal ductus arteriosus appears to be similar to the contiguous main pulmonary artery and descending aorta there are important histological differences, however. Histology and Mechanisms of Normal Closure Customer Service and Ordering Information.Journal of the American Heart Association (JAHA).

Stroke: Vascular and Interventional Neurology.Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).

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