Pressure-related capillary leukostasis following ischemia-reperfusion and hemorrhagic shock.
Pressure-related capillary leukostasis following ischemia-reperfusion and hemorrhagic shock.
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缺血再灌注和失血性休克后与压力相关的毛细血管白细胞停滞。
DOI：
10.1152/ajpheart.1993.265.1.h381
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Arfors,KE
中科院分区：
文献类型：
--
作者：
Hansell,P;Borgstrom,P;Arfors,KE
尽管对白细胞黏附的受体依赖性静脉黏附已有较好的描述，但对毛细血管白血球淤滞知之甚少。用荧光活体显微镜观察兔肌缺血再灌注或出血后毛细血管内白细胞的变化。定容出血或全脑缺血4h后，毛细血管后静脉壁可见纤维断裂、水肿、白细胞渗出、边际化等炎性损伤。然而，只要动脉灌流压在27至72毫米汞柱之间，毛细血管白细胞停滞的频率就很低(4-8个/mm2)，并且在所有组中都是相似的，包括用抗黏附抗体IB4治疗的动物。相反，当灌流压降到20毫米汞柱时，对照组(有或没有IB4)和缺血组的毛细血管白血球停滞增加相似(16-21个/mm2)。此外，当灌流压力增加到27毫米汞以上时，静止的白细胞(27-72毫米汞柱)恢复到原来的低水平(4-5个/毫米~2)。这些结果与以下结论一致，即在某些炎性损伤中，毛细血管白细胞停滞是一种与压力相关的现象，不依赖于受体，并且在早期恢复灌流压力后是自由可逆的。
Although the receptor-dependent venular adhesion of leukocyte adherence has been relatively well characterized, less is known about capillary leukostasis. With the use of fluorescence intravital microscopy, leukocyte behavior in the capillaries of rabbit tenuissimus muscle was evaluated after ischemia-reperfusion or hemorrhage. After fixed volume hemorrhage or 4 h of total ischemia, inflammatory injury was manifest by broken fibrils, edema, leukocyte infiltration, and margination along the postcapillary venular walls. Nevertheless, as long as arterial perfusion pressure was between 27 and 72 mmHg, the frequency of capillary leukostasis was low (4-8 cells/mm2) and similar in all groups, including animals treated with the antiadhesion antibody IB4. In contrast, when perfusion pressure decreased to 20 mmHg, capillary leukostasis increased similarly (to 16–21 cells/mm2) in controls (with or without IB4) and in those subjected to ischemia. Furthermore, when perfusion pressure was increased to more than 27 mmHg, (27–72 mmHg) stationary leukocytes returned to the original low level (4–5 cells/mm2). These results are consistent with the conclusion that during some inflammatory injuries, capillary leukostasis is a pressure-related phenomena that is not receptor dependent and is freely reversible with the early restoration of perfusion pressure.