The effect of fetal urine on the development of the bowel in gastroschisis.

A gastroschisis model was successfully developed in the chicken embryo. The embryologic anatomy of this laboratory animal enabled the inducement of an abdominal wall defect, whereby the eviscerated abdominal contents were not exposed to fetal urine. A total of 999 embryos underwent a surgical intervention at an early developmental stage, from the 5th-8th day of the incubation period. Twenty-four hour mortality was 7%. Surgery carried out on the 5th day resulted in the largest number of survivors, 25% of the induced lesions had healed and gastroschisis did not occur. The characteristic picture of gastroschisis only evolved when the herniated bowel was exposed to urine components. Histologic studies were carried out with the aid of various staining techniques to determine the development and distribution of the enteric ganglia in experimental gastroschisis. Contrary to similar studies that would point to damage of enteric ganglion cells as being responsible for the delay in intestinal motility, no ganglionic injury was noted in our bowel studies.