The effects of PAF antagonist on intestinal mucosal microcirculation after burn in rats

Gut originated infection (GOI) has been recognized as a potential factor for postburn irreversible shock, early sepsis and multiple system organ failure[1-5]. The intestinal mucosal barrier injury has been implicated as the cause of postburn GOI[6-8]. However, pathogenesis of the lesion is not well known. Platelet activating factor (PAF), an endogenous phospholipid mediator, has recently been proposed as an important mediator of postburn intestinal mucosal barrier injury and gut originated infection[9-11]. But the mechanism of PAF is not well defined. In this study, we have evaluated sequential hemodynamic changes in the intestinal mucosa after burn injury and investigated the role of PAF by assessing whether pretreatment against intestinal mucosal hemodynamic disturbance and pathologic damage, so as to further explore the role and its mechanism of PAF in postburn intestinal mucosal barrier injury.