Venous endothelial damage produced by massive sticking and emigration of leukocytes.
Venous endothelial damage produced by massive sticking and emigration of leukocytes.
复制标题
白细胞大量粘附和迁移造成静脉内皮损伤。
作者：
G. Stewart;W. G. Ritchie;P. Lynch
对犬颈静脉和股静脉的扫描和透射电子显微镜研究表明，大量白细胞粘附在血管壁上，穿过内皮细胞间连接并积累在内皮和基底膜之间的袋中。这导致内皮细胞广泛分离和脱落，许多区域内皮下结构暴露。白细胞侵入是由于邻近组织（而不是血管本身）受到手术创伤，随后在解剖区域下方施加外部压力导致 1 或 7 分钟闭塞所致。利多卡因（Xylocaine）可阻断侵袭，利多卡因是一种已知能抑制白细胞迁移的药物。然而，当利多卡因治疗的狗的静脉灌注正常血液时，就会发生白细胞侵袭。用长春碱使中性粒细胞减少的狗没有发生白细胞侵袭，但当这些静脉灌注正常血液时却发生了白细胞侵袭。
A scanning and transmission electron microscope study of canine jugular and femoral veins revealed that large numbers of white cells adhered to the vessel walls, passed through the endothelial intercellular junctions and accumulated in pockets between the endothelium and basement membrane. This led to extensive separation and desquamation of endothelial cells with exposure of subendothelial structures in many areas. The white cell invasion was caused by surgical trauma to adjacent tissues (rather than to the vessel itself) followed by 1 or 7 minutes occlusion by pressure applied externally just below the areas of dissection. The invasion was blocked by lidocaine (Xylocaine), an agent known to inhibit white cell migration. However, white cell invasion occurred when veins in lidocaine-treated dogs were perfused with normal blood. No white cell invasion occurred in dogs made neutropenic with vinblastine but did occur when these veins were perfused with normal blood.