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Models of persistent pulmonary hypertension of the newborn (PPHN) and the role of cyclic guanosine monophosphate (GMP) in pulmonary vasorelaxation.

Abstract
At birth, a marked decrease in pulmonary vascular resistance allows the lung to establish gas exchange. Persistent pulmonary hypertension of the newborn (PPHN) occurs when this normal adaptation of gas exchange does not occur. We review animal models used to study the pathogenesis and treatment of PPHN. Both acute models, such as acute hypoxia and infusion of vasoconstrictors, and chronic models of PPHN created both before and immediately after birth are described. Inhaled nitric oxide is an important emerging therapy for PPHN. We review nitric oxide receptor mechanisms, including soluble guanylate cyclase, which produces cGMP when stimulated by nitric oxide, and phosphodiesterases, which control the intensity and duration of cGMP signal transduction. A better understanding of these mechanisms of regulation of vascular tone may lead to safer use of nitric oxide and improved clinical outcomes.
AuthorsR H Steinhorn, F C Morin 3rd, J R Fineman
JournalSeminars in perinatology (Semin Perinatol) Vol. 21 Issue 5 Pg. 393-408 (Oct 1997) ISSN: 0146-0005 [Print] United States
PMID9352612 (Publication Type: Journal Article, Review)
Chemical References
  • Nitric Oxide Synthase
  • Cyclic GMP
Topics
  • Animals
  • Constriction, Pathologic
  • Cyclic GMP (biosynthesis, physiology)
  • Disease Models, Animal
  • Humans
  • Hypertension, Pulmonary (physiopathology)
  • Hypoxia
  • Infant, Newborn
  • Ligation
  • Nitric Oxide Synthase (antagonists & inhibitors)
  • Persistent Fetal Circulation Syndrome (physiopathology)
  • Pulmonary Artery (pathology, physiopathology)
  • Vasodilation

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