The role of amniotic fluid ingestion on the development of various fetal organic systems was evaluated in the rabbit model. The fetuses from 24 New Zealand white rabbits were studied on the 23rd day of gestation. Right ovarian-end fetuses underwent esophageal ligation (EL) or sham (SH) operations. Rabbits were submitted to hysterectomy on gestational day 30, and various organic systems of live fetuses were examined by weight and histological evaluations. Additionally, small intestinal enzymes were determined. Three fetal deaths, one in EL and two in SH groups, occurred with a total survival rate of 85%. EL resulted in increased amniotic fluid volume. Although fetal body weights (BW), lung, heart, liver and renal weights and liver weight/BW, lung weight/BW ratios did not differ, gastric, small intestinal and total gastrointestinal tract weights significantly decreased in EL group (p < 0.05). Additionally, gastric weight/BW, small intestinal weight/BW, total gastrointestinal tract weight/BW and renal weight/BW ratios were also significantly decreased (p < 0.01). Sucrase and maltase activities were not detectable in either group. Lactase activity in proximal small intestinal tissue was significantly decreased in EL group (p < 0.05). Mid and distal small intestinal tissue lactase activities did not reveal any significant difference among groups. Histologically, alveolar enlargement and alveolar thickening in fetal lungs, decreased glomerular count and tubular degeneration in fetal kidneys, and slight changes in fetal livers such as cellular vacuolization and reduction in central vein count were observed in the fetuses with esophageal ligation. While small intestinal tissues showed no marked changes, fetal stomach tissues in EL group revealed marked histological alterations consistent with erosive gastritis. This study suggests that amniotic fluid ingestion has no important effects on fetal somatic growth but effects the development of various fetal organic systems. Since the nutritional role of amniotic fluid is obscure, changes in amniotic fluid dynamics, and/or impairment of release of some possible fetal organotrophic factors, and/or unused states of the organs may be responsible for the morphologic changes secondary to esophageal ligation.