Guo W, Swaniker F, Fonkalsrud E W, Vo K, Karamanoukian R
Division of Pediatric Surgery, UCLA School of Medicine 90024, USA.
J Pediatr Surg. 1995 Jul;30(7):983-6; discussion 986-7. doi: 10.1016/0022-3468(95)90326-7.
Infants with gastroschisis experience delayed intestinal motility and absorption for several weeks after birth. This intestinal dysfunction is believed to occur primarily in the third trimester and to be largely caused by the prolonged exposure of the intestine to amniotic fluid. Previous studies have shown that prenatal steroid administration will enhance mucosal disaccharidase activity and nutrient uptake. The present study evaluates the effects of dexamethasone on intestinal function in a rabbit fetal gastroschisis model. Thirty-four fetuses from 10 New Zealand white rabbits were divided into three groups: (1) gastroschisis group (GSC, n = 10), gastroschisis was created on gestational day (GD) 24 (term = 31 to 33 days); (2) dexamethasone group (GSD, n = 10), after the creation of gastroschisis, a small osmotic pump was placed into the rabbit doe for dexamethasone infusion into the fetal amniotic cavity for 7 days (0.2 microgram/g/d); (3) normal group (NF, n = 10), unoperated littermates from the GSC group. There were no maternal deaths, and fetal survival rate was 85%. The fetal small intestinal disaccharidase enzyme, lactase (UE/g protein), was markedly decreased in GSC fetuses. It was increased 70% in the GSD group but lower than in normal fetuses (GSC = 10.0 +/- 1.6; GSD = 17.3 +/- 1.6 [GSD versus GSC, P < .05]; NF = 48.0 +/- 6.7). Maltase activity in the GSD group was significantly increased (GSC = 7.2 +/- 1.1; GSD = 13.9 +/- 1.8 [GSD versus GSC, P < .05]; NF = 12.2 +/- 1.3).(ABSTRACT TRUNCATED AT 250 WORDS)
