Intestinal damage due to gastroschisis (G), an anomaly found with increasing incidence by pedriatic surgeons, is intimately associated with endogenous nitric oxide (NO) production and NO synthase (NOS) expression. Aim: Aim of the study was to evaluate NO production and NOS isoforms in the intestine and amniotic fluid (AF) using a rat model of gastroschisis. Methods: A gastroschisis rat model was surgically created at 18.5 days of gestation (term=22 days). 3 groups of 12 fetuses each were studied: control (C), sham (S) and (G). Morphometric data of body weight (BW), intestinal weight (IW) and the IW/BW ratio were evaluated and compared. Indirect quantification of NO (nitrite and nitrate NOx) was analyzed by chemiluminescence, and the expression of the 3 isoforms was analyzed by Western blotting. Results: Group G showed an increase in IW and IW/BW compared with groups C and S. IW: G=0.270.06, C=0.200.02, S=0.200.02 (p<0.01); IW/BW: G=4.110.57, C=5.211.04, S=5.181.23 (p<0.05). NO in the G group was lower in the intestine and higher in AF, as opposed to C and S, where it had increased in the intestine and decreased in AF. Intestinal NOx: G=0.850.28, C=1.860.82, S=1.800.69 (p<0.05); NOx in AF: G=161.8752.11, C=6.995.45, S=48.7313.183 (p<0.001). Conclusion: The intestinal inflammation in gastroschisis promotes the release of nitric oxide to the environment (AF). Perhaps NO in the AF may be an inflammatory marker for G.
- amniotic fluid
- experimental surgery
- nitric oxide synthases
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health