Wilson L M, Baldwin A L
Department of Physiology, College of Medicine, University of Arizona, Tucson 85724-5051, USA.
Microcirculation. 1999 Sep;6(3):189-98.
Mental stress has been shown to produce intestinal disease, but the effects of a mild environmental stress on intestinal physiology have not been elucidated. This study was performed to determine the effects of environmental stress on the ultrastructure of the intestinal mucosa, using the rat as an experimental model.
One group of rats (group A, n = 3) was examined immediately upon arrival at the animal care facility. Groups B (n = 6) and C (n = 6) were housed in rooms with high and low personnel activity, respectively, for up to 4 wk. Group D (n = 8) was housed in the high activity room for 3 to 4 wk followed by 1, 2, or 3 in the low activity room.
Rats in group B had the greatest number of degranulated intestinal mucosal mast cells, and activated goblet cells. Intestinal villi were edematous and epithelial cells were detaching from the basement membrane at villus tips. Changes were observed in capillary endothelial ultrastructure. In group B there were greater numbers of vesicles and multilamellar fenestral diaphragms compared to group C. Rats in groups A and C had the lowest numbers of degranulated mast cells and activated goblet cells. Intestinal villi showed normal ultrastructure. Group D was in a recovery phase and the condition of the intestinal mucosa was improved relative to group B, but the number of degranulated mast cells was not significantly reduced.
This study demonstrates that environmentally induced stress causes pathological changes in the rat intestinal mucosa that compromise the epithelial-endothelial exchange barrier. These results emphasize the importance of closely monitoring the environment of experimental animals and provide evidence to stimulate further research into the mechanisms linking mental stress to gastrointestinal dysfunction in humans.
精神压力已被证明会引发肠道疾病，但轻度环境压力对肠道生理的影响尚未阐明。本研究以大鼠为实验模型，旨在确定环境压力对肠道黏膜超微结构的影响。
一组大鼠（A组，n = 3）在抵达动物护理设施后立即进行检查。B组（n = 6）和C组（n = 6）分别饲养在人员活动频繁和稀少的房间中，长达4周。D组（n = 8）先在人员活动频繁的房间饲养3至4周，然后在人员活动稀少的房间饲养1、2或3周。
B组大鼠肠道黏膜脱颗粒肥大细胞和活化杯状细胞数量最多。肠绒毛水肿，绒毛尖端的上皮细胞从基底膜脱落。毛细血管内皮超微结构出现变化。与C组相比，B组有更多的囊泡和多层窗孔隔膜。A组和C组大鼠脱颗粒肥大细胞和活化杯状细胞数量最少。肠绒毛显示正常超微结构。D组处于恢复阶段，肠道黏膜状况相对于B组有所改善，但脱颗粒肥大细胞数量未显著减少。
本研究表明，环境诱导的压力会导致大鼠肠道黏膜发生病理变化，损害上皮 - 内皮交换屏障。这些结果强调了密切监测实验动物环境的重要性，并为进一步研究精神压力与人类胃肠功能障碍之间的联系机制提供了证据。
