Etiology of intestinal damage in gastroschisis. III: Morphometric analysis of the smooth muscle and submucosa.

The response of intestinal smooth muscle to injury may explain some of the motility derangement observed in infants with gastroschisis. An experimental model of gastroschisis was created and a detailed analysis of the intestinal muscle layer was undertaken to study this response. An abdominal wall defect and evisceration of the bowel were carried out in fetal lambs at 80 days' gestation (full term, 145 days), with delivery at 100 days or 135 days. Smooth muscle cell size and number were determined by detailed morphometric analysis, proliferative rate was determined using proliferating cell nuclear antigen staining, and collagen content was determined by morphometry after Verhoeff van Gieson staining. Compared with controls, there was a significant increase in cell number (hyperplasia) in the gastroschisis animals at 100 days and an increase in size (hypertrophy) at 135 days. The proliferation rate of smooth muscle was significantly lower and the submucosal collagen thickness was significantly greater in the gastroschisis animals during both periods. These data suggest that gastroschisis is characterised by initial hyperplasia, with subsequent diminution in smooth muscle proliferation. The hypertrophy may reflect a response to injury in which cell growth instead of proliferation occurs. The persistent elevation in collagen throughout gestation in animals with gastroschisis may be a reflection of this hyperplastic response in the smooth muscle cells and an important factor in the bowel-wall thickening. This deranged pattern of growth may lead to the clinical problems observed in human infants with this disease.