Yao Y M, Redl H, Bahrami S, Schlag G
Trauma Research Center, 304th Hospital, Postgraduate Medical College, Beijing, China.
Inflamm Res. 1998 May;47(5):201-10. doi: 10.1007/s000110050318.
Multiple alterations in inflammatory and immunologic function have been demonstrated in clinical and experimental situations after trauma and hemorrhage, in particular the activation of various humoral (e.g. complement, coagulation) and cellular systems (neutrophils, endothelial cells, macrophages). As a consequence of this activation process there is synthesis, expression and release of numerous mediators (toxic oxygen species, proteolytic enzymes, adherence molecules, cytokines), which may produce a generalized inflammation and tissue damage in the body. Mediators are responsible for ongoing interactions of different cell types and for amplification effects through their networks and feedback cycles, finally leading to a sustained inflammation and multiple organ damage in the body. In the setting of trauma/shock, many activators including bacterial as well as non-bacterial factors may be present that will induce local and systemic inflammatory responses. Although the potential role of bacteria/endotoxin translocation and its clinical relevance remains controversial, many lines of evidence support the concept that the gut may be the reservoir for systemic sepsis and subsequent MOF in a number of pathophysiologic states.
在创伤和出血后的临床及实验情况下，已证实炎症和免疫功能存在多种改变，尤其是各种体液系统（如补体、凝血系统）和细胞系统（中性粒细胞、内皮细胞、巨噬细胞）的激活。作为这种激活过程的结果，会合成、表达和释放大量介质（毒性氧物质、蛋白水解酶、黏附分子、细胞因子），这些介质可能在体内引发全身性炎症和组织损伤。介质负责不同细胞类型之间的持续相互作用，并通过其网络和反馈循环产生放大效应，最终导致体内持续炎症和多器官损伤。在创伤/休克情况下，可能存在许多激活剂，包括细菌及非细菌因素，它们会诱导局部和全身炎症反应。尽管细菌/内毒素移位的潜在作用及其临床相关性仍存在争议，但许多证据支持这样的概念，即在多种病理生理状态下，肠道可能是全身性脓毒症及随后多器官功能衰竭的根源。
