TREATMENT DURING LATE PREGNANCY WITH ACE INHIBITORS MIMICS BRONCHOPULMONARY DYSPLASIA IN PRETERM BORN ANIMALS

CONFORTI ROCIO AYELEM; CIUFFO GM; SOLER GARCIA FLORENCIA M; FUENTES LB; SANCHEZ SUSANA INES

Mendoza

Congreso; XXXIV REUNION CIENTIFICA ANUAL DE LA SOCIEDAD DE BIOLOGIA DE CUYO; 2016

Sociedad de Biología de Cuyo

Preterm birth affects 8-10% of human pregnancies. Individuals born preterm, especially if they develop bronchopulmonary dysplasia (BPD), have an increased risk of impaired lung function in infancy, childhood and adulthood. The etiology of BPD is multifactorial. Genetic susceptibility and environmental factors have all been implicated in the etiology of BPD. The renin-angiotensin system (RAS) during fetal or neonatal stages has been involved in lung growth and differentiation process.The present study tests the hypothesis that exposureduring critical stages of lung developmentto ACE inhibitorscould be associated with alterations in pulmonary structure that mimics human BPD.Pregnant Wistar rats were administered subcutaneously(osmoticmini-pumps, Alzet)during late gestation (E13-E21) with captopril or enalapril (2,85 mg/kg/day) and lungs from their offspring were analyzed at P0, P8 and P15 postnatal ages.We performed an histological and morphometric analyses, as well as immunolocalization of proliferating cell nuclear antigen (PCNA). At the different ages, animals showedimpaired alveolarization,hyperplasia of airway smooth muscle and increased muscularization of pulmonary vessels.These anatomical changes were present as early as P0with both treatments. Differences between treatments were observed with regard to the level of PCA.This model could be useful in understanding the pathogenesis of BPD and to define therapies to ameliorate human BPD.