Histochemical studies of experimental fetal intestinal obstruction.
Experimental intestinal atresia can be produced by mesenteric disruption in fetal lambs. In previous reports, a detailed histochemical study of the bowel in this atresia model demonstrated: (1) hyperplasia of ganglion cells in the dilated proximal segment, (2) involutional changes in the area of maximal distension, (3) decreased to absent adenosine triphosphatase (ATP-ase) production in the area of the atresia, (4) gradual increase of ATP-ase production to normal proximally, and (5) greater reduction of ATP-ase production along the antimesenteric border compared to the mesenteric border. In the present study, a model of fetal intestinal obstruction by simple ligation of the bowel has been created to observe the effects of pure obstruction of the lumen of the fetal bowel without the possible ischemic effects of any vascular interruption. Studies with this model reveal: (1) hyperplasia of ganglion cells in the dilated proximal segment, and (2) decreased ATP-ase production proximal to the obstruction, but (3) no involutional changes in the area of maximal distension. These findings show a pattern of disturbance of bowel morphology and function caused by obstruction of the fetal bowel that is similar to but less severe than that seen with intestinal atresia.
D000110:Acetylcholinesterase / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D005315:Fetal Diseases / Q000209:etiology / Q000378:metabolism*; D007409:Intestinal Atresia / Q000150:complications; D007415:Intestinal Obstruction / Q000209:etiology / Q000378:metabolism*; D011247:Pregnancy; D012756:Sheep
D000110:Acetylcholinesterase; D000251:Adenosine Triphosphatases