Background: In congenital diaphragmatic hernia (CDH), vascular pulmonary underdevelopment could induce severe pulmonary hypertension; however, its significance in perinatal ventricular load conditions is largely unknown. Ventricular pressure overload induces increased myocardium gene expression of B-type natriuretic peptide (BNP), components of the renin-angiotensinogen and endothelin (ET)–1 system. Our aim was to evaluate perinatal myocardium expression of these genes in a nitrofen-induced CDH rat model.

Methods: In the nitrofen-induced CDH rat model, fetuses from dated pregnant Sprague-Dawley rats at 15.5, 17.5, 19.5 and 21.5 days postcoitum as well as newborn pups were assigned to 3 experimental groups: control, nitrofen (exposed to nitrofen, without CDH), and CDH (exposed to nitrofen, with CDH). Myocardial samples collected from the right and left ventricle were processed for quantification of mRNA of BNP, angiotensinogen, and ET-1.

Results: The perinatal expression of BNP, angiotensinogen, and ET-1 mRNA in the right and left ventricle of the control group revealed daily changes. During gestation, the expression of BNP and angiotensinogen mRNA underwent significant oscillation compared with control in both nitrofen-exposed fetuses, although there is no significant differences between the nitrofen and CDH groups. After birth, occurs a significant increasing expression of all studied genes only in the right ventricle of CDH pups.

Conclusions: The pre-natal myocardial quantification of BNP, angiotensinogen, and ET-1 mRNA demonstrated that CDH is only associated with significant molecular alterations in the right ventricle and after birth, suggesting that vascular alterations does not have significant pre-natal impact in fetal hemodynamic.