Upperman J S, Deitch E A, Guo W, Lu Q, Xu D
Department of Surgery, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103, USA.
Shock. 1998 Dec;10(6):407-14. doi: 10.1097/00024382-199812000-00005.
The goal of these experiments was to test the hypothesis that after a nonlethal episode of hemorrhagic shock, factors carried in the mesenteric lymph would promote endothelial cell injury and activate neutrophils to a greater extent than portal vein plasma. Catheters were placed in the efferent lymphatic duct draining the mesenteric lymph node complex, after which male rats were subjected to sham or actual shock (30 mmHg for 90 min), and lymph was collected. Portal vein plasma was collected from the sham-shock and shocked rats at 6 h post-shock or sham-shock. When the effect of lymph or portal blood plasma was tested on endothelial cell (HUVEC) monolayer permeability, it was found that post-shock lymph, but not post-shock portal vein plasma, increased HUVEC permeability to both 10 kDa and 40 kDa permeability probes. Subsequent experiments documented that only post-shock lymph was cytotoxic to endothelial cells as manifest both by decreased trypan blue dye exclusion and the increased release of Chromium-51 from chromium-loaded endothelial cells. Furthermore post-shock lymph induced a greater increase in neutrophil superoxide formation than pre-shock lymph, pre-shock, or post-shock portal vein plasma. Lastly, neutrophil-mediated endothelial cell injury was potentiated by the presence of post-shock lymph, and the magnitude of HUVEC injury was greater in endothelial cells incubated with post-shock lymph plus neutrophils than in monolayers incubated with post-shock lymph or neutrophils alone. These results suggest that post-shock lymph is cytotoxic to endothelial cells and activates neutrophils. Since the lung is the first organ that is exposed to mesenteric lymph, lung injury after hemorrhagic shock may be mediated by factors contained in mesenteric lymph.
在非致死性失血性休克发作后，肠系膜淋巴中携带的因子比门静脉血浆更能促进内皮细胞损伤并激活中性粒细胞。将导管置于引流肠系膜淋巴结复合体的输出淋巴管中，之后对雄性大鼠进行假手术或实际休克（30 mmHg，持续90分钟），并收集淋巴液。在休克或假休克后6小时，从假休克和休克大鼠中收集门静脉血浆。当检测淋巴液或门静脉血浆对内皮细胞（人脐静脉内皮细胞）单层通透性的影响时，发现休克后淋巴液而非休克后门静脉血浆增加了人脐静脉内皮细胞对10 kDa和40 kDa通透性探针的通透性。后续实验证明，只有休克后淋巴液对内皮细胞具有细胞毒性，这表现为锥虫蓝染料排斥减少以及铬负载的内皮细胞中铬-51释放增加。此外，休克后淋巴液比休克前淋巴液、休克前或休克后门静脉血浆诱导中性粒细胞超氧化物形成的增加更大。最后，休克后淋巴液的存在增强了中性粒细胞介导的内皮细胞损伤，与单独用休克后淋巴液或中性粒细胞培养的单层相比，用休克后淋巴液加中性粒细胞培养的内皮细胞中人脐静脉内皮细胞损伤的程度更大。这些结果表明，休克后淋巴液对内皮细胞具有细胞毒性并激活中性粒细胞。由于肺是第一个接触肠系膜淋巴的器官，失血性休克后的肺损伤可能由肠系膜淋巴中所含的因子介导。
