作者: Frederick A Moore
DOI: 10.1016/S0002-9610(99)00231-7
关键词: Shock (circulatory) 、 Systemic inflammatory response syndrome 、 Gastrointestinal tract 、 Mechanism (biology) 、 Pathogenesis 、 Proinflammatory cytokine 、 Immunology 、 Sepsis 、 Refractory shock 、 Medicine
摘要: Despite intensive investigation, the pathogenesis of postinjury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly implicate that gastrointestinal tract plays a pivotal role. Shock with resulting gut hypoperfusion appears to be one important inciting event. While early studies persuasively focused attention on bacterial translocation as unifying mechanism explain late sepsis syndromes characterize MOF, subsequent suggest other gut-specific mechanisms are operational. Based our Trauma Research Center observations those others, we conclude that: 1) may contribute refractory shock; 2) for patients who survive shock, reperfused source proinflammatory mediators amplify systemic inflammatory response syndrome; 3) sets stage progressive dysfunction such becomes reservoir pathogens toxins MOF.