RESUMO
UNLABELLED: Intestinal damage due to gastroschisis (G), an anomaly found with increasing incidence by pediatric 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=0.27 ± 0.06, C=0.20 ± 0.02, S=0.20 ± 0.02 (p<0.01); IW/BW: G=4.11 ± 0.57, C=5.21 ± 1.04, S=5.18 ± 1.23 (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=0.85 ± 0.28, C=1.86 ± 0.82, S=1.80 ± 0.69 (p<0.05); NOx in AF: G=161.87 ± 52.11, C=6.99 ± 5.45, S=48.73 ± 13.183 (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.
