Pickard L R, Santoro S, Wyllie R G, Haller J A
J Pediatr Surg. 1981 Jun;16(3):256-60. doi: 10.1016/s0022-3468(81)80675-6.
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.
实验性肠闭锁可通过破坏胎羊的肠系膜来诱发。在以往的报告中，对该闭锁模型中的肠道进行的详细组织化学研究表明：（1）扩张的近端段神经节细胞增生；（2）最大扩张区域出现退化性改变；（3）闭锁区域三磷酸腺苷酶（ATP酶）产生减少至缺失；（4）近端ATP酶产生逐渐增加至正常水平；（5）与肠系膜缘相比，沿反肠系膜缘的ATP酶产生减少更明显。在本研究中，通过简单结扎肠道建立了胎儿肠梗阻模型，以观察单纯胎儿肠腔梗阻的影响，而不存在任何血管中断可能带来的缺血影响。对该模型的研究显示：（1）扩张的近端段神经节细胞增生；（2）梗阻近端ATP酶产生减少；但（3）最大扩张区域无退化性改变。这些发现表明，胎儿肠道梗阻引起的肠道形态和功能紊乱模式与肠闭锁所见相似，但程度较轻。
