Abstract
Persistent pulmonary hypertension of the newborn (PPHN) is the failure of the pulmonary circulation to adapt successfully to postnatal conditions. Associated with a wide variety of neonatal cardiopulmonary disorders, PPHN represents the inability to achieve or sustain a drop in pulmonary vascular resistance during the immediate newborn period. Previous clinical and experimental studies suggested that intrauterine events may play important roles in its pathogenesis. Supportive evidence includes: (1) the timing of onset of disease within hours of birth; (2) the severity of histologic findings at autopsy of infants with severe PPHN dying within the first few days, including marked smooth muscle and perivascular adventitial thickening;1 and (3) animal studies suggesting that fetal stresses, such as hypoxia or hypertension, can cause smooth muscle thickening of small pulmonary arteries.
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