Vascular Endothelial Mitochondrial Function Predicts Death or Pulmonary Outcomes in Preterm Infants

Vascular endothelial mitochondrial dysfunction contributes to the pathogenesis of several oxidant stress-associated disorders. Oxidant stress is a major contributor to the pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity that often leads to sequelae in adult su...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2017-10, Vol.196 (8), p.1040-1049
Main Authors: Kandasamy, Jegen, Olave, Nelida, Ballinger, Scott W, Ambalavanan, Namasivayam
Format: Article
Language:English
Subjects:
Bioenergetics
Birth weight
Bronchopulmonary Dysplasia - etiology
Bronchopulmonary Dysplasia - mortality
Bronchopulmonary Dysplasia - physiopathology
Deoxyribonucleic acid
DNA
Female
Humans
Hydrogen peroxide
Hyperoxia
Hypertension
Infant, Extremely Premature - physiology
Infant, Newborn
Infant, Premature - physiology
Male
Mitochondrial Diseases - etiology
Mitochondrial Diseases - mortality
Mitochondrial Diseases - physiopathology
Mitochondrial DNA
Mortality
Newborn babies
Original
Oxidative stress
Pathogenesis
Premature babies
Premature birth
Respiration, Artificial - adverse effects
Rodents
United States
Vascular Diseases - etiology
Vascular Diseases - mortality
Vascular Diseases - physiopathology
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Summary:Vascular endothelial mitochondrial dysfunction contributes to the pathogenesis of several oxidant stress-associated disorders. Oxidant stress is a major contributor to the pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity that often leads to sequelae in adult survivors. This study was conducted to identify whether differences in mitochondrial bioenergetic function and oxidant generation in human umbilical vein endothelial cells (HUVECs) obtained from extremely preterm infants were associated with risk for BPD or death before 36 weeks postmenstrual age. HUVEC oxygen consumption and superoxide and hydrogen peroxide generation were measured in 69 infants. Compared with HUVECs from infants who survived without BPD, HUVECs obtained from infants who developed BPD or died had a lower maximal oxygen consumption rate (mean ± SEM, 107 ± 8 vs. 235 ± 22 pmol/min/30,000 cells; P 
ISSN:1073-449X
1535-4970
DOI:10.1164/rccm.201702-0353OC