ABSTRACT
OBJECTIVE: Changes in nutritional strategies over the past decade have been shown to improve postnatal growth in extremely low birth weight (ELBW) infants. We showed 10 years ago that the majority of these ELBW infants with bronchopulmonary dysplasia (BPD) suffer postnatal growth failure. We theorized that recent changes in nutritional support strategies would positively affect growth outcomes in ELBW infants with BPD. STUDY DESIGN: A retrospective study of 88 ELBW infants with BPD. Nutritional data, postnatal growth and BPD severity were compared across three cohorts: (1) weight gain ≤14 g kg(-1) per day, (2) 14.1 to 16 g kg(-1) per day and (3) ≥16 g kg(-1) per day from return to birth weight through discharge. We also compared these to a historical cohort. RESULT: In all, 73% of current subjects grew at or above fetal rates. There was less extrauterine growth restriction (EUGR) by weight and head circumference for those ELBW infants with BPD receiving higher amounts of protein. Aggressive early TPN and receipt of caloric-dense milk seemed to be the 'new' nutritional strategies improving growth for current ELBW infants with BPD compared with those 10 years ago. CONCLUSION: Despite a diagnosis of BPD, improved nutritional strategies have enhanced postnatal growth in infants at high risk for EUGR.
Subject(s)
Bronchopulmonary Dysplasia/epidemiology , Infant, Extremely Low Birth Weight , Nutritional Requirements , Weight Gain , Bronchopulmonary Dysplasia/diagnosis , Bronchopulmonary Dysplasia/therapy , Chi-Square Distribution , Cohort Studies , Female , Follow-Up Studies , Humans , Infant Nutritional Physiological Phenomena , Infant, Newborn , Intensive Care Units, Neonatal , Linear Models , Male , Nutritional Support , Respiration, Artificial/methods , Retrospective Studies , Risk Assessment , Time FactorsABSTRACT
AIM: Lung ischaemia-reperfusion induces nitric oxide synthesis and reactive nitrogen species, decreasing nitric oxide bioavailability. We hypothesized that in the ventilated lung, this process begins during ischaemia and intensifies with reperfusion, contributing to ischaemia-reperfusion-induced pulmonary vasoconstriction. The aim was to determine whether ischaemia-reperfusion alters inducible and endothelial nitric oxide synthase expression/activity, reactive nitrogen species generation, and nitric oxide bioavailability, potentially affecting pulmonary perfusion. METHODS: Ischaemia-reperfusion was induced for various times in anesthetized rabbits with ventilated lungs by reversibly occluding the right pulmonary artery and initiating reperfusion. Nitric oxide synthase activity/expression and phosphorylation, reactive nitrogen species generation and total nitrate/nitrite were determined in lung tissue. RESULTS: Inducible nitric oxide synthase expression and activity, and reactive nitrogen species formation coincided with increased pulmonary vascular resistance during reperfusion and increased with ischaemia duration, further increasing after 2-h reperfusion. Total nitrate/nitrite also increased with ischaemia but decreased after 2-h reperfusion. Pre-treatment with an inducible nitric oxide synthase inhibitor (1400W; Cayman Chemical Company, Ann Arbor, MI, USA) attenuated inducible nitric oxide synthase activity, reactive nitrogen species generation and pulmonary vascular resistance, but did not affect total nitrate/nitrite. Endothelial nitric oxide synthase expression was unchanged by ischaemia-reperfusion; however, its phosphorylation on serine 1177 and dephosphorylation on threonine 495 was uncoupled, suggesting decreased endothelial nitric oxide synthase activity. 1400W prevented uncoupling of endothelial nitric oxide synthase phosphorylation, maintaining its activity during reperfusion. CONCLUSION: Ischaemia-reperfusion up-regulates inducible nitric oxide synthesis and/activity, which coincides with reduced endothelial nitric oxide synthase activity as suggested by its uncoupling and may contribute to ischaemia-reperfusion-induced pulmonary vasoconstriction.
