Treatment of multiple oragn dysfunction syndrom : establisment of endothelial cell targetting therapy

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Microcirculatory insufficiency resulting from endothelial cell injury is a main causative factor in sepsis-induced multiple organ dysfunction syndrome, which is a main cause of death in critical care unit. In this study, we sought to determine if endothelial cell growth factor therapy decrease organ injury in sepsis model. In in vitro experiments, we examined whether angiogenic factors such as basic fibroblast growth factor ad vascular endotthelial cell growth factor can Inhibit endothelial cell injury induced by reactive oxygen Intermediates or activated neutrophils. In 3-dimensional culture model, we showed that treatment with bFGF and VEGF could attenuate the decrease in tube formation of endothelial cells. We also demonstrated that anti-oxidative stress reagent such as N-acetyl cystein can Inhibit mitochondrial dysfunction In endothelial cells Induced by activated neutrophils and reactive oxygens such as hydrogen peroxide. In animal sepsis model, we examined the effects of angiogenic factors administration could attenuate the oorgan injury such as liver dysfunction. However we could not show the therapeutic effect of angiogenic factors administration on liver injury in this sepsis model. We are going to use both angiogenic factors and bone marrow cells for treatment of septic liver injury and oragn regeneration in animal model.