Basic and clinical studies asociated with hepatic reticulo endothelial system after major surgery

建立了一种稳定的失血性休克复苏实验动物模型，用于严重感染(败血症)或肝功能衰竭的基础研究。研究各脏器功能障碍的过程，并用该模型客观评价肝脏网状内皮功能。在该模型中，获得了与多器官衰竭密切相关的全身炎症反应综合征的证据，即终末期器官损伤和终末期脓毒症，表明该休克模型对模拟脓毒症和器官衰竭是有用的。尤其是肝功能衰竭。我们还证明了器官损伤。尤其是肝功能衰竭，与微循环功能不全和炎性细胞(如中性粒细胞)聚集有关。因此，我们得出结论，阻断这些因素可能是治疗器官损伤的重要关键。从概念上讲，肝脏网状内皮功能是对细菌感染(如大肠杆菌感染)的主要宿主防御系统，我们部分阐明了这种免疫反应在肝脏中的确切机制。此外，我们还阐明了一氧化氮(NO)。它是一种强大的血管扩张剂，调节有机微循环，保护器官免受损害，参与肝脏细菌的杀灭。然而。140被认为具有细胞损伤的作用。因此，选择性一氧化氮合酶的调节有望预防大手术后的肝功能障碍。

A stable hemorrhagic shock-resuscitation model of experimental animals for the basic study of severe infection (sepsis) or hepatic failure was established. The process of each organ dysfunction were studied and the hepatic reticuloendothelial function was objectively evaluated using our model. In this model, the evidence of systemic inflammatory response syndrome which is closely associated with multiple organ failure known as ultimate organ injury and terminal stage of sepsis were obtained, indicating that this shock model is useful to simulate sepsis and organ failure. especially hepatic failure. We also demonstrated that the organ injury. Especially hepatic failure, were associated with microcirculatory insufficiency and the accumulation of inflammatory cells (e.g. neutrophils). We, therefore, concluded that the blockage against these factors was likely to the important key for the treatment of the organ injury. The hepatic reticuloendothelial function is conceptually major host defense system to the bacterial infection such as E.coli infection and we partly elucidated the precise mechanisms of this immune response in the liver. Additionally, we elucidated that nitric oxide (NO). which is strong vaso-dilator regulating the organic microcirculation to protect from organ damages, is to be involved in bacterial killing in the liver. Whereas. 140 are recognized to have the effect of cellular injury. Therefore, regulation of selective NO synthetase would be expected to prevent hepatic dysfunction after major operation.