Wagner R
Fortschr Med. 1980 Jul 26;98(28):1077-82.
After ligationof the vascular arcades of the upper jejunum in rats ischemic damage to the intestinal mucosa and its regenerative behavior were investigated by histology, morphometry, enzyme-histochemistrym, autoradiography and electron microscopy. The process of ischemic damage begins at the tips of the villi and progresses to the crypts. After ischemia lasting 300 min the mucosa, submucosa and muscularis propria are necrotic, which means, that the small intestine is at this time completely infarcted. Whilst sthe ischemic damage to the crypt epithelia is similar to that of other kinds of epithelia, the ischemic damage to the enterocytes is different. The enterocytes are shed to the intestinal lumen without any signs of irreversible damage by a blebformation at their cell base. After 2 h ischemia -- the basal epithelia of the crypts are not irreversible damaged yet at this time--and a 12 h period of restored blood flow, the mucosal surface is completely covered again by a flat epithelium. This is achieved 1) by an above-normal proliferation of the epithelia derived from the residual crypts, 2) by the appearance of flat epithelia with an increased diameter. After 8 days of repair the small intestinal mucosa shows morphologically, autoradiographically and enzyme-histochemically a normal picture again.
在结扎大鼠空肠上段的血管弓后，通过组织学、形态计量学、酶组织化学、放射自显影和电子显微镜研究了肠黏膜的缺血性损伤及其再生行为。缺血性损伤过程始于绒毛顶端，并向隐窝发展。缺血持续300分钟后，黏膜、黏膜下层和固有肌层发生坏死，这意味着此时小肠已完全梗死。虽然隐窝上皮的缺血性损伤与其他类型上皮的损伤相似，但肠上皮细胞的缺血性损伤有所不同。肠上皮细胞通过其细胞基部形成泡状结构而脱落至肠腔，且无任何不可逆损伤的迹象。缺血2小时后（此时隐窝的基底上皮尚未发生不可逆损伤），再经过12小时的血流恢复，黏膜表面再次被扁平上皮完全覆盖。这是通过以下方式实现的：1）来自残留隐窝的上皮细胞异常增殖；2）出现直径增大的扁平上皮。修复8天后，小肠黏膜在形态学、放射自显影和酶组织化学方面再次呈现正常状态。
