Takase Shinya, Lerond Laurence, Bergan John J, Schmid-Schönbein Geert W
Department of Bioengineering and The Whitaker Institute for Biomedical Engineering, University of California-San Diego, La Jolla, California 92093-0412, USA.
Am J Physiol Heart Circ Physiol. 2002 Apr;282(4):H1387-94. doi: 10.1152/ajpheart.01003.2000.
Elevated venous pressure can be associated with severe tissue injury. Few links, however, between venous hypertension and tissue damage have been established. We examined here the effects of micropressure elevation on the outcome of venular occlusion/reperfusion in the mesenteric microvasculature of male Wistar rats. One hour of venular occlusion (diameter approximately 50 microm) by micropipette occlusion followed by reperfusion were carried out with sham surgery without occlusion as control. Leukocyte rolling, adhesion, and migration, oxygen radicals detected by dichlorofluorescein (DCF), and parenchymal cell death detected by propidium iodide (PI) were recorded simultaneously in the same vessel at a location upstream of the occlusion site with elevated micropressure and at a downstream location with low micropressure. The number of rolling, adhering, and migrating leukocytes increased on the upstream side of the occlusion to a higher level than downstream of the occlusion site. During occlusion, DCF intensity on the venular endothelium was greater on the upstream side than in the downstream side, but there were no differences during reperfusion. The number of PI-positive cells adjacent to the venules increased significantly compared with controls, and it remained greater on the upstream higher-pressure side than the downstream side. Leukocyte adhesion and transvascular migration in postcapillary venules as well as parenchymal cell death could be significantly reduced by the hydroxyl radical scavenger dimethylthiourea. Microhemorrhages of blood cells into the mesentery interstitium were observed only on the upstream side of the occlusion. These results indicate that an elevation of the venular blood pressure during occlusion/reperfusion exacerbates the inflammatory cascade and tissue injury. Venous occlusion may constitute an important mechanism for tissue injury.
静脉压升高可能与严重的组织损伤有关。然而，静脉高压与组织损伤之间的联系鲜有确立。我们在此研究了微压力升高对雄性Wistar大鼠肠系膜微血管中小静脉闭塞/再灌注结果的影响。通过微量移液器闭塞小静脉（直径约50微米）1小时后再灌注，以未进行闭塞的假手术作为对照。在闭塞部位上游微压力升高处和下游微压力较低处的同一血管中，同时记录白细胞滚动、黏附及迁移情况，用二氯荧光素（DCF）检测氧自由基，用碘化丙啶（PI）检测实质细胞死亡情况。与闭塞部位下游相比，闭塞部位上游滚动、黏附及迁移的白细胞数量增加至更高水平。在闭塞期间，小静脉内皮上的DCF强度在上游侧大于下游侧，但在再灌注期间无差异。与对照组相比，小静脉附近PI阳性细胞数量显著增加，且在上游高压侧仍多于下游侧。羟基自由基清除剂二甲基硫脲可显著减少毛细血管后微静脉中的白细胞黏附和跨血管迁移以及实质细胞死亡。仅在闭塞部位的上游观察到血细胞向肠系膜间质的微出血。这些结果表明，闭塞/再灌注期间小静脉血压升高会加剧炎症级联反应和组织损伤。静脉闭塞可能是组织损伤的一个重要机制。
