Pathogenetic effects of platelet activating factor on enterogenic endotoxemia after burn

Previous clinical and experimental studies have indicated that an early endotoxemia occurred after a major burn. It is unlikely that burn wound sepsis is the source of circulating endotoxin in less than 12 h after burn. Increasing evidence demonstrates that the bacteria and endotoxin in the gastrointestinal tract can pass through the gut barrier into blood circulation to form enterogenic endotoxemia following burn[1-3]. However, its pathogenesis remains poorly understood. Platelet activating factor (PAF), an endogenous phospholipid mediator, has recently been proposed as a critical mediator in shock, sepsis and multiple organ failure[4,5]. In this study, the relationship between changes of PAF and enterogenic endotoxemia was observed on rat models with 30% TBSA III burn. The purpose was to investigate the pathogenetic effects of PAF on the occurrence of enterogenic endotoxemia after burn.