Gut-derived mesenteric lymph but not portal blood increases endothelial cell permeability and promotes lung injury after hemorrhagic shock
Gut-derived mesenteric lymph but not portal blood increases endothelial cell permeability and promotes lung injury after hemorrhagic shock
复制标题
DOI：
10.1097/00000658-199810000-00008
复制
发表时间：
1998-10-01
影响因子：
9
通讯作者：
Deitch, EA
中科院分区：
文献类型：
--
作者：
Magnotti, LJ;Upperman, JS;Deitch, EA
目的探讨失血性休克大鼠肠系膜淋巴液中肠源性因子的水平是否高于门静脉血中肠源性因子的水平。这一假设进行了测试，通过检查门静脉血浆和肠系膜淋巴对内皮细胞单层和肠系膜淋巴液流休克诱导的肺injury.Summary背景DataThe检测菌血症或内毒素血症的创伤受害者的门静脉血中的情况下中断的影响，怀疑肠道在多器官功能衰竭的产生的作用。尽管如此，以前的实验工作已经清楚地证明了休克和肠道损伤之间的联系，以及肠道诱导的脓毒症和远端器官衰竭的概念。对这一明显矛盾的一种解释是肠源性炎症因子通过肠循环而不是门静脉循环到达肺和体循环。方法将培养在二室系统中的人脐静脉内皮细胞单层暴露于培养基、假休克或休克后门静脉血浆或淋巴液中，并测定其对罗丹明（10 K）的通透性。对Sprague-Dawley大鼠进行90分钟的假休克或实际休克和休克加淋巴分裂（休克前后）。肺通透性，肺髓过氧化物酶水平，肺泡细胞凋亡，支气管肺泡液蛋白含量被用来定量肺injury.ResultsPostshock淋巴液增加内皮细胞单层通透性，但不postshock血浆，假休克淋巴/血浆，或介质。失血性休克前的淋巴分裂可防止休克诱导的肺对伊文思蓝染料的通透性增加和肺泡细胞凋亡，并降低肺MPO水平。与此相反，分裂的肠系膜血管在休克期结束，但再灌注改善，但未能防止肺通透性增加，肺泡细胞凋亡，MPO accumulation.ConclusionsGut屏障功能衰竭后失血性休克可能参与休克引起的远端器官损伤的发病机制，通过肠源性因子进行肠系膜淋巴，而不是门静脉循环。
ObjectiveTo determine whether gut-derived factors leading to organ injury and increased endothelial cell permeability would be present in the mesenteric lymph at higher levels than in the portal blood of rats subjected to hemorrhagic shock. This hypothesis was tested by examining the effect of portal blood plasma and mesenteric lymph on endothelial cell monolayers and the interruption of mesenteric lymph flow on shock-induced lung injury.Summary Background DataThe absence of detectable bacteremia or endotoxemia in the portal blood of trauma victims casts doubt on the role of the gut in the generation of multiple organ failure. Nevertheless, previous experimental work has clearly documented the connection between shock and gut injury as well as the concept of gut-induced sepsis and distant organ failure. One explanation for this apparent paradox would be that gut-derived inflammatory factors are reaching the lung and systemic circulation via the gut lymphatics rather than the portal circulation. Methods Human umbilical vein endothelial cell monolayers, grown in two-compartment systems, were exposed to media, shamshock, or postshock portal blood plasma or lymph, and permeability to rhodamine (10K) was measured. Sprague-Dawley rats were subjected to 90 minutes of sham or actual shock and shock plus lymphatic division (before and after shock). Lung permeability, pulmonary myeloperoxidase levels, alveolar apoptosis, and bronchoalveolar fluid protein content were used to quantitate lung injury.ResultsPostshock lymph increased endothelial cell monolayer permeability but not postshock plasma, sham-shock lymph/plasma, or medium. Lymphatic division before hemorrhagic shock prevented shock-induced increases in lung permeability to Evans blue dye and alveolar apoptosis and reduced pulmonary MPO levels. In contrast, division of the mesenteric lymphatics at the end of the shock period but before reperfusion ameliorated but failed to prevent increased lung permeability; alveolar apoptosis, and MPO accumulation.ConclusionsGut barrier failure after hemorrhagic shock may be involved in the pathogenesis of shock-induced distant organ injury via gut-derived factors carried in the mesenteric lymph rather than the portal circulation.