Effect of Artificial Ventilation on Pulmonary Antioxidant Enzyme Activities in a Congenital Diaphragmatic Hernia Rat Model

Abstract

Treatment of infants with congenital diaphragmatic hernia (CDH) developing respiratory insufficiency within a few hours after birth remains unsatisfactory. The incidence of CDH is about 1:3000 newborns (Hazebroek et al, 1988), mortality for these high-risk infants ranges from 30%-60%. These infants require aggressive respiratory support, including high pressures and oxygen concentrations. Frequently the clinical course is complicated by pulmonary hypertension. Compared to premature infants, CDH survivors have a high incidence (40%) of bronchopulmonary dysplasia (BPD) (Molenaar et al, 1991; Redmond et al, 1987; O’Rourke et al, 1991). Because this disease occurs almost exclusively in premature infants who receive mechanical ventilation with increased inspiratory oxygen concentration, it was postulated (Northway et al, 1967; Crapo, 1986) that oxygen alone is toxic to the lung parenchyma. Other factors that may play a role in BPD include gestational age, barotrauma, infection, the presence of a persistent ductus arteriosus (PDA), pulmonary hypertension and reperfusion damage. It is difficult to separate the effect of oxygen from those of other factors that may influence the development of BPD. Therefore the need for a reliable animal model (preferably with CDH) to study the pathogenesis of BPD and investigate protective measurements has augmented. DeLuca described barotrauma in ventilated CDH lambs; there was no specific mention of oxygen toxicity or its defense mechanisms (DeLuca et al, 1987).