Abstract
Unlike in the adult, the perinatal/neonatal pulmonary vascular response to chronic hypoxic exposure is much more rapid and severe and results in the failure of the fetal/neonatal circulation to adapt to a response supporting postnatal life. This, in turn, contributes to the pathogenesis of persistent pulmonary hypertension of the newborn and pulmonary vascular dysfunction later in life. As such, furthering our understanding of the mechanisms and pathology of perinatal/neonatal pulmonary hypertension development leading to adult diseases is important to support more effective therapeutic target identification.
Highlights
The role of stromal cell-derived factor 1 (SDF-1) and chemokine receptor type 4 (CXCR4) in neonatal hypoxia-induced pulmonary hypertension has been described [7,8]
This study suggests that chronic hypoxia in utero results in increased vasopressor response to both acute hypoxia and serotonin, but that rho-kinase is involved only in the increased response to serotonin
Muscarinic M1 ACh receptor (AChR) mRNA expression was increased in lungs and pulmonary arteries of mice born in hypoxia
Summary
The role of stromal cell-derived factor 1 (SDF-1) and chemokine receptor type 4 (CXCR4) in neonatal hypoxia-induced pulmonary hypertension has been described [7,8]. *Corresponding author: Qiwei Yang, Department of Pediatrics, College of Medicine, University of Illinois at Chicago, USA, Tel: 312-413-8502; E-mail: qiwei@uic.edu Received January 10, 2014; Accepted January 11, 2014; Published January 18, 2014 Pressure during acute hypoxic exposure compared to low altitude lambs [12].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
