Department of Anatomy & Cell Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
Cell Tissue Res. 2011 Feb;343(2):411-9. doi: 10.1007/s00441-010-1096-z. Epub 2010 Dec 14.
Periods of ischemia followed by restoration of blood flow cause ischemia/reperfusion (I/R) injury. In the intestine, I/R damage to the mucosa and neurons is prominent. Functionally, abnormalities occur in motility, most conspicuously a slowing of transit, possibly as a consequence of damage to neurons and/or muscle. Here, we describe degenerative and regenerative changes that have not been previously reported in intestinal muscle. The mouse small intestine was made ischemic for 1 h, followed by re-perfusion for 1 h to 7 days. The tissues were examined histologically, after hematoxylin/eosin and Masson's trichrome staining, and by myeloperoxidase histochemistry to detect inflammatory reactions to I/R. Histological analysis revealed changes in the mucosa, muscle, and neurons. The mucosa was severely but transiently damaged. The mucosal surface was sloughed off at 1-3 h, but re-epithelialization occurred by 12 h, and the epithelium appeared healthy by 1-2 days. Longitudinal muscle degeneration was followed by regeneration, but little effect on the circular muscle was noted. The first signs of muscle change were apparent at 3-12 h, and by 1 and 2 days, extensive degeneration within the muscle was observed, which included clear cytoplasm, pyknotic nuclei, and apoptotic bodies. The muscle recovered quickly and appeared normal at 7 days. Histological evidence of neuronal damage was apparent at 1-7 days. Neutrophils were not present in the muscle layers and were infrequent in the mucosa. However, they were often seen in the longitudinal muscle at 1-3 days and were also present in the circular muscle. Neutrophil numbers increased in the mucosa in both I/R and sham-operated animals and remained elevated from 1 h to 7 days. We conclude that I/R causes severe longitudinal muscle damage, which might contribute to the long-term motility deficits observed after I/R injury to the intestine.
缺血期随后恢复血流会导致缺血/再灌注（I/R）损伤。在肠道中，黏膜和神经元的 I/R 损伤很明显。在功能上，运动出现异常，最明显的是转运速度减慢，这可能是神经元和/或肌肉损伤的结果。在这里，我们描述了以前在肠道肌肉中没有报道过的退行性和再生性变化。将小鼠小肠缺血 1 小时，然后再灌注 1 小时至 7 天。用苏木精/伊红和 Masson 三色染色后，通过髓过氧化物酶组织化学检测 I/R 引起的炎症反应，对组织进行组织学检查。组织学分析显示黏膜、肌肉和神经元发生变化。黏膜受到严重但短暂的损伤。黏膜表面在 1-3 小时脱落，但在 12 小时内重新上皮化，1-2 天内上皮看起来健康。纵行肌退化后再生，但对环形肌影响不大。肌肉变化的最初迹象在 3-12 小时出现，1 天和 2 天后，观察到肌肉内广泛退化，包括细胞质透明、核固缩和凋亡小体。肌肉恢复迅速，7 天后恢复正常。1-7 天可见神经元损伤的组织学证据。在肌肉层中没有中性粒细胞，在黏膜中也很少见。然而，它们在 1-3 天的纵行肌中经常出现，在环形肌中也存在。在 I/R 和假手术动物的黏膜中，中性粒细胞数量增加，从 1 小时到 7 天都保持升高。我们得出结论，I/R 导致严重的纵行肌损伤，这可能是 I/R 损伤肠道后观察到的长期运动缺陷的原因。
