Boros M, Takaichi S, Masuda J, Newlands G F, Hatanaka K
Department of Etiology/Pathophysiology, National Cardiovascular Center Research Institute, Osaka, Japan.
Shock. 1995 Feb;3(2):125-31.
The goals of this study were to investigate the in vivo effects of intestinal ischemia-reperfusion on mucosal mast cells, and to evaluate the morphological changes induced by standardized arterial occlusion in anesthetized rats. Complete segmental ileal ischemia was maintained for 15, 30, or 60 min, and was followed by a 30 min reperfusion period. Intestinal biopsies taken at the end of ischemia and in the 30th min of reperfusion were evaluated by image analysis, and the rate of release of type II rat mast cell protease, a marker of mast cell exocytosis, was determined from the venous effluent of the segment. Electron microscopy revealed cytoplasmic vacuolization of the mast cells of the villi after the 15 min ischemia. Ischemia induced a continuous diminution of the mucosal thickness and a significant fall in the number of mast cells in the villi; with immunoperoxidase staining with a monoclonal antibody that recognizes the AD1 mast cell surface antigen, the decrease was 57, 49, and 66% in the 15, 30, and 60 min ischemia groups, respectively. In these groups, the mucosal type II mast cell protease concentration increased to 2.4-, 2.5-, and 3.6-fold, respectively, and a significant increase in plasma protease levels was observed on reperfusion. These results lead us to conclude that mucosal mast cells are very sensitive to intestinal ischemia, with the majority of mast cells in the ileal villi already involved in the response to ischemia after a short period of arterial occlusion.
本研究的目的是探讨肠道缺血再灌注对黏膜肥大细胞的体内影响,并评估麻醉大鼠标准化动脉闭塞诱导的形态学变化。完全节段性回肠缺血持续15、30或60分钟,随后进行30分钟的再灌注期。在缺血结束时和再灌注第30分钟采集的肠道活检组织通过图像分析进行评估,并从该节段的静脉流出物中测定II型大鼠肥大细胞蛋白酶(肥大细胞胞吐作用的标志物)的释放率。电子显微镜显示,缺血15分钟后绒毛的肥大细胞出现细胞质空泡化。缺血导致黏膜厚度持续减小,绒毛中肥大细胞数量显著下降;用识别AD1肥大细胞表面抗原的单克隆抗体进行免疫过氧化物酶染色,在缺血15、30和60分钟组中,肥大细胞数量分别减少了57%、49%和66%。在这些组中,黏膜II型肥大细胞蛋白酶浓度分别增加到2.4倍、2.5倍和3.6倍,再灌注时血浆蛋白酶水平显著升高。这些结果使我们得出结论,黏膜肥大细胞对肠道缺血非常敏感,在短时间动脉闭塞后,回肠绒毛中的大多数肥大细胞已参与对缺血的反应。