Ravnic Dino J, Konerding Moritz A, Tsuda Akira, Huss Harold T, Wolloscheck Tanja, Pratt Juan P, Mentzer Steven J
Laboratory of Immunophysiology, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA.
Gut. 2007 Apr;56(4):518-23. doi: 10.1136/gut.2006.101824. Epub 2006 Nov 17.
Blood flowing across the vascular endothelium creates wall shear stress, dependent on velocity of flow and vessel geometry, that tends to disrupt lymphocyte-endothelial cell adhesion.
The microcirculation in a murine model of acute colitis was investigated to identify structural adaptations during acute colitis that may facilitate transmigration.
In 2,4,6-trinitrobenzenesulphonic acid-induced acute colitis, the infiltrating cells and colonic microcirculation was investigated by cellular topographic mapping, corrosion casting and three-dimensional scanning electron microscopy (SEM). Colonic blood velocimetry was performed using intravital microscopy.
Clinical and histological parameters suggested a peak inflammatory response at 96 h (p<0.001). The infiltrating cells were spatially related to the mucosal capillary plexus by three-dimensional topographic mapping (p<0.001). In normal mice, corrosion casting and three-dimensional SEM showed a polygonal mucosal plexus supplied by ascending arteries and descending veins. After 2,4,6-trinitrobenzenesulphonic acid stimulation, three-dimensional SEM showed preserved branch angles (p = 0.52) and nominal vessel lengths (p = 0.93), but a significantly dilated mucosal capillary plexus (p<0.001). Intravital microscopy of the mucosal plexus showed a greater than twofold decrease in the velocity of flow (p<0.001).
The demonstrable slowing of the velocity of flow despite an increase in volumetric flow suggests that these microvascular adaptations create conditions suitable for leucocyte adhesion and transmigration.
流经血管内皮的血液会产生壁面剪应力,其取决于血流速度和血管几何形状,该剪应力往往会破坏淋巴细胞与内皮细胞的黏附。
研究急性结肠炎小鼠模型中的微循环,以确定急性结肠炎期间可能促进细胞迁移的结构适应性变化。
在2,4,6-三硝基苯磺酸诱导的急性结肠炎中,通过细胞拓扑绘图、铸型腐蚀和三维扫描电子显微镜(SEM)研究浸润细胞和结肠微循环。使用活体显微镜进行结肠血流速度测定。
临床和组织学参数表明在96小时时炎症反应达到峰值(p<0.001)。通过三维拓扑绘图发现浸润细胞在空间上与黏膜毛细血管丛相关(p<0.001)。在正常小鼠中,铸型腐蚀和三维SEM显示由升动脉和降静脉供应的多边形黏膜丛。在2,4,6-三硝基苯磺酸刺激后,三维SEM显示分支角度保持不变(p = 0.52),血管标称长度不变(p = 0.93),但黏膜毛细血管丛明显扩张(p<0.001)。对黏膜丛进行活体显微镜观察发现血流速度下降超过两倍(p<0.001)。
尽管容积流量增加,但血流速度明显减慢,这表明这些微血管适应性变化创造了适合白细胞黏附和迁移的条件。