Abstract
Persistent Pulmonary Hypertension of the newborn (PPHN) is the clinical syndrome that is characterized by the failure to achieve or sustain pulmonary vasodilation at birth, leading to severe hypoxemia due to extrapulmonary right-to-left shunting of blood across the foramen ovale and ductus arteriosus. As a potent and selective pulmonary vasodilator, inhaled NO (iNO) has been shown to be an effective therapy for PPHN. However, some infants have limited or no response to iNO therapy, leading to the need for ECMO therapy or death. Mechanisms that contribute to poor responses to iNO in some infants with PPHN are incompletely understood, but are partly related to impairment of NO-cGMP signalling in the hypertensive neonatal pulmonary circulation. Based on past studies that demonstrated impaired production of endogenous nitric oxide (NO) in PPHN, we hypothesized that BAY 412272, a direct soluble guanylate cyclase (sGC) activator, may be a potent pulmonary vasodilator in the perinatal pulmonary circulation, thereby providing a novel treatment strategy for severe PPHN.
Highlights
Persistent Pulmonary Hypertension of the newborn (PPHN) is the clinical syndrome that is characterized by the failure to achieve or sustain pulmonary vasodilation at birth, leading to severe hypoxemia due to extrapulmonary right-to-left shunting of blood across the foramen ovale and ductus arteriosus
Mechanisms that contribute to poor responses to inhaled nitric oxide (NO) (iNO) in some infants with PPHN are incompletely understood, but are partly related to impairment of NO-cGMP signalling in the hypertensive neonatal pulmonary circulation
Based on past studies that demonstrated impaired production of endogenous nitric oxide (NO) in PPHN, we hypothesized that BAY 412272, a direct soluble guanylate cyclase activator, may be a potent pulmonary vasodilator in the perinatal pulmonary circulation, thereby providing a novel treatment strategy for severe PPHN
Summary
Persistent Pulmonary Hypertension of the newborn (PPHN) is the clinical syndrome that is characterized by the failure to achieve or sustain pulmonary vasodilation at birth, leading to severe hypoxemia due to extrapulmonary right-to-left shunting of blood across the foramen ovale and ductus arteriosus. NO-cGMP signaling in the pathogenesis and treatment of persistent pulmonary hypertension of the newborn Email: Steven H Abman* - steven.abman@uchsc.edu * Corresponding author from 2nd International Conference of cGMP Generators, Effectors and Therapeutic Implications Potsdam, Germany, 10–12 June, 2005
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