Prostaglandin synthesis inhibition in persistent pulmonary hypertension of the newborn.
The data implicating prostaglandin synthesis inhibitors as an etiology for PPHN are reviewed. Consideration is given to the pharmacology of prostaglandin synthesis inhibitors in the fetus and newborn, the role of prostaglandins in the fetal and neonatal circulation, and the effect of closure of the ductus arteriosus on the fetal pulmonary vasculature.
D000818:Animals; D001794:Blood Pressure; D004374:Ductus Arteriosus, Patent / Q000503:physiopathology; D005260:Female; D005333:Fetus / Q000187:drug effects; D006801:Humans; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism; D007213:Indomethacin / Q000009:adverse effects*; D007231:Infant, Newborn; D008168:Lung / Q000098:blood supply / Q000378:metabolism; D009288:Naproxen / Q000009:adverse effects*; D010547:Persistent Fetal Circulation Syndrome / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism; D011247:Pregnancy; D011453:Prostaglandins / Q000096:biosynthesis* / Q000502:physiology; D011652:Pulmonary Circulation; D012459:Salicylates / Q000009:adverse effects*; D012756:Sheep; D014661:Vasoconstriction
D011453:Prostaglandins; D012459:Salicylates; D009288:Naproxen; D007213:Indomethacin