The ductus arteriosus normally closes within the first 48 hours of life by spasm of muscle within its walls. The patency of the ductus during interuterine life is due to the combined effects of low oxygen partial pressure and locally synthesized prostaglandins.
Following birth, the pulmonary resistance falls and the systemic vascular resistance rise due to cessation of the placental circulation. Hence, aortic pressure exceeds right ventricular pressure. Flow through the ductus reverses for several days, becoming left-to-right.
The increased oxygen partial pressure stimulates muscular contraction within the wall of the vessel. There may be a reduction in synthesis of prostaglandin E. Bradykinin is released by the lungs during their first inflation; this also triggers spasm of the muscle within the walls of the ductus.
After a couple of months, complete closure of the ductus is achieved by proliferation of its intima.
This automatic closure mechanism is less likely to work in very premature babies, those with respiratory distress or those with perinatal asphyxia.
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