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Pathophysiologic mechanisms of persistent pulmonary hypertension of the newborn
Author(s) -
Dakshinamurti S.
Publication year - 2005
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.20201
Subject(s) - medicine , hypoxia (environmental) , pulmonary hypertension , cardiology , context (archaeology) , pathophysiology , sepsis , endothelial dysfunction , paleontology , chemistry , organic chemistry , oxygen , biology
Persistent pulmonary hypertension of the newborn (PPHN), among the most rapidly progressive and potentially fatal of vasculopathies, is a disorder of vascular transition from fetal to neonatal circulation, manifesting as hypoxemic respiratory failure. PPHN represents a common pathway of vascular injury activated by numerous perinatal stresses: hypoxia, hypoglycemia, cold stress, sepsis, and direct lung injury. As with other multifactorial diseases, a single inciting event may be augmented by multiple concurrent/subsequent phenomena that result in differing courses of disease progression. I review the various mechanisms of vascular injury involved in neonatal pulmonary hypertension: endothelial dysfunction, inflammation, hypoxia, and mechanical strain, in the context of downstream effects on pulmonary vascular endothelial‐myocyte interactions and myocyte phenotypic plasticity. © 2005 Wiley‐Liss, Inc.