Abstract 1911

Background: Heart hypoplasia is present in infants with CDH, being related to survival. We study the effects of prenatal exposure on heart development in fetal rats with CDH induced by nitrofen.

Material and methods: At 9.5 day gestation, dams received either olive oil (n=2) or 100 mg nitrofen (n=12). Latter, three nitrofen-fed dams were treated with dexamethasone (0.25 mg/Kg) on days 18 and 19. Three groups of fetuses were studied: control (n=21), nitrofen-exposed with hernia (CDH, n=41), and dexamethasone-treated fetuses with hernia (DEX, n=12). At 21 days, the fetal hearts were recovered, weighted, frozen and protein and DNA contents were determined. One-way ANOVA were used for statistical analysis. p<0.05 was used as level of significance.

Results: In comparison to control group, heart weight (35±3 vs 21±4 mg) and heart weight/body weight ratio (6.5±0.7 vs. 5.2±0.8 mg/g) were decreased in CDH fetuses. Also, protein and DNA contents (1.6±0.4 mg, 65±15 µg, respectively) were significantly lower than controls (2.3±0.4 mg, 86±15 µg). In comparison to CDH group, DEX group showed an increase of heart weight (25±3 mg), heart weight/body weight ratio (5.8±0.7 mg/g) and DNA content (126±10 µg), but did not reach values similar to controls.

Conclusions: CDH induced by nitrofen produces heart hypoplasia (low heart weight, heart weight/body weight ratio) and an adverse effect on cellular growth (decreased DNA and protein contents). Prenatal dexamethasone exposure partially reverse heart hypoplasia by increasing cell proliferation.

Supported by grants: G.V. 96/0059-2; FIS 96/0059.