What is the functional and anatomic closure process of the ductus arteriosus?

Updated: Nov 20, 2018
  • Author: Luke K Kim, MD; Chief Editor: Stuart Berger, MD  more...
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In the fetus, the oxygen tension is relatively low, because the pulmonary system is nonfunctional. Coupled with high levels of circulating prostaglandins, this acts to keep the ductus open. The high levels of prostaglandins result from the little amount of pulmonary circulation and the high levels of production in the placenta.

At birth, the placenta is removed, eliminating a major source of prostaglandin production, and the lungs expand, activating the organ in which most prostaglandins are metabolized. In addition, with the onset of normal respiration, oxygen tension in the blood markedly increases. Pulmonary vascular resistance decreases with this activity.

Normally, functional closure of the ductus arteriosus occurs by about 15 hours of life in healthy infants born at term. This occurs by abrupt contraction of the muscular wall of the ductus arteriosus, which is associated with increases in the partial pressure of oxygen (PO2) coincident with the first breath. A preferential shift of blood flow occurs; the blood moves away from the ductus and directly from the right ventricle into the lungs. Until functional closure is complete and PVR is lower than SVR, some residual left-to-right flow occurs from the aorta through the ductus and into the pulmonary arteries.

This was first demonstrated by multiple experiments in the 1940s and has been subsequently confirmed. Although the neonatal ductus appears to be highly sensitive to changes in arterial oxygen tension, the actual reasons for closure or persistent patency are complex and involve manipulation by the autonomic nervous system, chemical mediators, and the ductal musculature.

A balance of factors that cause relaxation and contraction determine the vascular tone of the ductus. Major factors causing relaxation are the high prostaglandin levels, hypoxemia, and nitric oxide production in the ductus. Factors resulting in contraction include decreased prostaglandin levels, increased PO2, increased endothelin-1, norepinephrine, acetylcholine, bradykinin, and decreased PGE receptors. Increased prostaglandin sensitivity, in conjunction with pulmonary immaturity leading to hypoxia, contributes to the increased frequency of patent ductus arteriosus (PDA) in premature neonates.

Although functional closure usually occurs in the first few hours of life, true anatomic closure, in which the ductus loses the ability to reopen, may take several weeks. A second stage of closure related to fibrous proliferation of the intima is complete in 2-3 weeks.

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