Tiffany A Moore1, Kendra K Schmid2, Ann Anderson-Berry3, Ann M Berger4. 1. College of Nursing, University of Nebraska Medical Center (UNMC), Omaha, NE, USA tamoore@unmc.edu. 2. College of Public Health Masters Programs, University of Nebraska Medical Center (UNMC), Omaha, NE, USA. 3. College of Medicine, University of Nebraska Medical Center (UNMC), Omaha, NE, USA. 4. College of Nursing, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
Abstract
BACKGROUND: The role of oxidative stress remains unclear in the multifactorial pathophysiologic mechanism of lung disease in preterm infants. AIMS: The aim of this study was to examine the associations among chronic lung disease (CLD), oxidative stress, and oxygen requirements in preterm infants. DESIGN: Prospective, longitudinal, and correlational design. SUBJECTS: Preterm infants born at <32 weeks' gestation (N = 31), median gestation of 29.0 weeks (range 24.9-31.7). MEASUREMENTS: The diagnosis of CLD was obtained from the medical record. Oxidative stress was measured using 8-hydroxydeoxyguanosine (8-OHdG) in the cord blood at birth and urine on Days 1 and 7. Oxygen requirements were measured using fraction of inspired oxygen (FIO2) recorded in the first hour after birth/admission and the average FIO2 during the first 12 hr and 7 days after birth. Descriptive statistics are presented. Comparison analyses were performed using Kruskal-Wallis and Fisher's exact tests. RESULTS: Infants with CLD (n = 12) had lower gestational age (p = .04) and weight (p = .04) at birth, more days on the ventilator (p = .004), and longer neonatal intensive care unit stay (p = .04) compared to infants without CLD (n = 19). CLD was associated with lower oxidative stress levels (p = .03) and higher oxygen requirements during the first 12 hr (p = .025) and on Day 7 (p = .001). Lower oxidative stress levels on Day 7 were associated with higher oxygen requirements in the first 12 hr (p = .01) and on Day 7 (p = .03). CONCLUSION: Our results linking CLD and higher oxygen requirements with low oxidative stress contradict previous reports. Findings identify a gap in knowledge for postresuscitation oxygen therapy in preterm infants and expose the role of oxidative stress from inflammation and intermittent hypoxia in the etiology of CLD.
BACKGROUND: The role of oxidative stress remains unclear in the multifactorial pathophysiologic mechanism of lung disease in preterm infants. AIMS: The aim of this study was to examine the associations among chronic lung disease (CLD), oxidative stress, and oxygen requirements in preterm infants. DESIGN: Prospective, longitudinal, and correlational design. SUBJECTS: Preterm infants born at <32 weeks' gestation (N = 31), median gestation of 29.0 weeks (range 24.9-31.7). MEASUREMENTS: The diagnosis of CLD was obtained from the medical record. Oxidative stress was measured using 8-hydroxydeoxyguanosine (8-OHdG) in the cord blood at birth and urine on Days 1 and 7. Oxygen requirements were measured using fraction of inspired oxygen (FIO2) recorded in the first hour after birth/admission and the average FIO2 during the first 12 hr and 7 days after birth. Descriptive statistics are presented. Comparison analyses were performed using Kruskal-Wallis and Fisher's exact tests. RESULTS:Infants with CLD (n = 12) had lower gestational age (p = .04) and weight (p = .04) at birth, more days on the ventilator (p = .004), and longer neonatal intensive care unit stay (p = .04) compared to infants without CLD (n = 19). CLD was associated with lower oxidative stress levels (p = .03) and higher oxygen requirements during the first 12 hr (p = .025) and on Day 7 (p = .001). Lower oxidative stress levels on Day 7 were associated with higher oxygen requirements in the first 12 hr (p = .01) and on Day 7 (p = .03). CONCLUSION: Our results linking CLD and higher oxygen requirements with low oxidative stress contradict previous reports. Findings identify a gap in knowledge for postresuscitation oxygen therapy in preterm infants and expose the role of oxidative stress from inflammation and intermittent hypoxia in the etiology of CLD.
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