Post-hemorrhagic shock mesenteric lymph is cytotoxic to endothelial cells and activates neutrophils

The goal of these experiments was to test the hypothesis that after a nonle thal 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 lymp hatic duct draining the mesenteric lymph node complex, after which male rat s were subjected to sham or actual shock (30 mmHg for 90 min), and lymph wa s collected. Portal vein plasma was collected from the sham-shock and shock ed 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 probe s. Subsequent experiments documented that only post-shock lymph was cytotox ic to endothelial cells as manifest both by decreased trypan blue dye exclu sion and the increased release of Chromium-51 from chromium-loaded endothel ial cells. Furthermore post-shock lymph induced a greater increase in neutr ophil superoxide formation than pre-shock lymph, pre-shock, or post-shock p ortal 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 pl us neutrophils than in monolayers incubated with post-shock lymph or neutro phils alone. These results suggest that post-shock lymph is cytotoxic to en dothelial cells and activates neutrophils. Since the lung is the first orga n that is exposed to mesenteric lymph, lung injury after hemorrhagic shock may be mediated by factors contained in mesenteric lymph.