Intrauterine disruption of mesenteric blood supply in fetal lambs has been shown to produce a consistently reliable type 3 intestinal atresia. Histochemical evaluation of surviving bowel in this model has shown a striking hyperplasia of ganglion cells in the dilated proximal segment with involutional changes in the area of maximal distention. ATPase production is completely absent in the area of atresia but gradually increases to normal with more proximal sampling. In order to correlate these findings to the human newborn, similar studies were performed on the proximal and distal resected specimens obtained during surgical correction. In both jejunal and ileal atresia there is a similar hyperplasia of ganglion cells with definite involutional changes in the area of maximal distention. ATPase concentration shows the same deficiency adjacent to the atresia with gradual increase more proximally. At each level of section the antimesenteric border is markedly more depleted than the corresponding mesenteric border. These findings suggest that there is an initial hyperplasia of peristaltic components in response to obstruction, however, as unrelieved distention continues, these hyperplastic cells undergo involution and lysis. Applying these findings to clinical experience, effective peristalsis can be expected to occur only if an anastomosis is placed proximal to the point of maximal distention. © 1979 Grune & Stratton, Inc.