Esophageal, Tracheal and Pulmonary Parenchymal Alterations in Experimental Esophageal Atresia and Tracheoesophageal Fistula

Abstract

Pulmonary complications are among the most important causes of morbidity and mortality in neonates with esophageal atresia and tracheofistula. We aimed to investigate the possible causes of respiratory complications encountered in esophageal atresia (EA) and tracheoesophageal fistula (TEF) in an experimental model. Sprague-Dawley fetal rats treated with adriamycin were used for the experiment. Time mated pregnant rats were given 1.75 mg/kg of adriamicyn intraperitoneally on days 6–9 of gestation. The fetuses were sacrified on day 21, weighed, and dissected under the surgical microscope. The animals were divided into four groups: (1) control group; (2) saline-injected group; (3) adriamycin-induced EA group, and (4) adriamycin administered but without development of EA. The lungs, esophagus, and trachea were excised and underwent histological examination. The mucosa of distal esophagus was thickened (p < 0.05); the submucosa was thinner (p < 0.05); and the muscular layer was thickened (p < 0.05) in fetuses with EA and TEF. In adriamycin-treated rats, in which EA and TEF developed, tracheal cartilage was loosened and formed into a D or C shape. The cartilage was fragmented into several segments on transverse sections in most fetuses. Alveolar septa were thin in lungs of fetus with EA and TEF (p < 0.05), without any fibrosis or evidence of parenchymal abnormality microscopically. Our findings suggest that respiratory complications may contribute to structural lesions in the trachea and particularly in the distal esophagus but not in the pulmonary parenchyma itself.

Lung hypoplasia in rats with esophageal atresia and tracheo–esophageal fistula

“…If the embryologic mechanisms of EA-TEF in infants and rats are similar and the malformations observed in the respiratory tract are identical, it is likely that failures of parenchymal development are also of the same nature in both settings. Previous studies on lung parenchyma in the adriamycin rat model found fairly normal canalicularsaccular patterns (48) and hypoplasia with reduced density of type I pneumocytes (49), although, unfortunately, the authors did not attempt to assess branching or lung mass.…”