Reeve D R
Br J Exp Pathol. 1977 Feb;58(1):63-77.
Chronic colonic ulcers in the rat were produced by the administration of a hydrogen peroxide enema. Lesions of up to 10 months' duration were obtained by this method and a selection was examined ultrastructurally. It was hoped that the study would reveal causes for the chronicity of the lesions. From previous work it appeared that there was no failure of epithelial migration from the edge of the wound. The majority of cells at the ulcer margins demonstrated features of regeneration similar to those seen in other tissues, and that there were no specific changes concomitant with chronic ulceration. The majority of epithelial cells at the ulcer edge showed features of differentiation which indicated that there was no obvious fault in this process so essential to the basic requirements of tissue repair. It is possible that chronicity is produced by a failure of the epithelio-mesenchymal interaction mechanisms which, potentiated by an ischaemia resulting from submucosal vascular damage, results in the consequential death of migrating epithelial cells. This hypothesis is supported by the appearance of a squamous metaplasia in the healing lesions, a process which is commonly attributed to a chronic inflammatory response which may be induced by a relative vascular insufficiency.
通过给大鼠灌肠过氧化氢来诱发慢性结肠溃疡。用这种方法获得了持续长达10个月的损伤，并对其中一部分进行了超微结构检查。希望该研究能揭示损伤慢性化的原因。从先前的研究工作来看，伤口边缘上皮细胞迁移并未出现障碍。溃疡边缘的大多数细胞表现出与其他组织中所见相似的再生特征，并且慢性溃疡化过程中没有伴随特异性变化。溃疡边缘的大多数上皮细胞呈现出分化特征，这表明在这个对组织修复基本需求至关重要的过程中没有明显缺陷。慢性化可能是由上皮-间充质相互作用机制的故障导致的，这种故障因黏膜下血管损伤引起的缺血而加剧，进而导致迁移的上皮细胞死亡。愈合损伤中出现的鳞状化生现象支持了这一假说，鳞状化生这一过程通常归因于可能由相对血管不足诱发的慢性炎症反应。
