The imbalance of endogenous nitric oxide and endothelin-1 in in very low birth weighing infants with patent ductus arteriosus

Introduction Patent ductus arteriosus (PDA) is due to the failure of the ductus arteriosus to close after birth, and its incidence being inversely related to gestational age and birth weight (1,2). The incidence of PDA in term infants has been estimated to be 57 per 100 000 live births, whereas every third preterm infant with a birth weight of 501 to 1500 g can be expected to have a persistent PDA, and in premature extremely low birth weight infants (< 1000g) it’s as high as 50-65% (3,4). The presence of a PDA allows continuous shunting of blood from the aorta to the pulmonary artery due to the higher blood pressure in the systemic circulation compared to the pulmonary circulation. Preterm newborns with PDA are at greater risk for the the different morbidities, such as bronchopulmonary dysplasia, hypotension, renal dysfunction, intraventricular hemorrhage (IVH), and periventricular leukomalacia (PVL) and for other perinatal complications (5,6,7,8).