AIM To explore the kinetic changes in plasma D(-)-lactate and lipopolyssccharide(LPS)levels,andinvestigate whether D(-)-lactate could be used as amarker of intestinal injury in rats following gut ischemia/reperfusion,burn,and acute necrotizing pancreatitis(ANP).METHODS Three models were developed in rats:① gutischemia/ reperfusion obtained by one hour of superiormesenteric artery occlusion followed by reperfusion;②severe burn injury created by 30% of total body surfacearea(TBSA)full-thickness scald burn;and ③ ANPinduced by continuous inverse infusion of sodiumtaurocholate and trypsin into main pancreatic duct.Plasma levels of D(-)-lactate in systemic circulation andLPS in portal circulation were measured by enzymatic-spectrophotometric method and limulus amebocyte lysate(LAL)test kit,respectively.Tissue samples of intestinewere taken for histological analysis.RESULTS One hour gut ischemia followed by reperfusioninjuries resulted in a significant elevation in plasma D(-)-lactate and LPS levels,and there was a significantcorrelation between the plasma D(-)-lactate and LPS(r=0.719,P<0.05).The plasma concentrations of D(-)-lactate and LPS increased significantly at 6h postburn,and there was also a remarkable correlation between them(r = 0.877,P < 0.01).D(-)-lactate and LPS levelselevated significantly at 2h after ANP,with a similarsignificant correlation between the two levels(r = 0.798,P < 0.01 ).The desquamation of intestine villi andinfiltration of inflammatory cells in the lamina propriawere observed in all groups.CONCLUSION The changes of plasma D(-)-lactate levelsin systemic blood paralleled with LPS levels in the portalvein blood.The measurement of plasma D(-)-lactatelevel may be a useful marker to assess the intestinalinjury and to monitor an increase of intestinal permeabilityand endotoxemia following severe injuries in early stage. AIM To explore the kinetic changes in plasma D (-) - lactate and lipopolyssccharide (LPS) levels, and investigate whether D (-) - lactate could be used as a marker of intestinal injury in rats following gut ischemia / reperfusion, burn, and acute necrotizing pancreatitis (ANP) .METHODS Three models were developed in rats: ① gutischemia / reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; ②severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and ③ ANPinduced by continuous inverse infusion of sodium torocholate and trypsin into main pancreatic duct. Plasma levels of D (-) - lactate in systemic circulation and LPS in portal circulation were measured by enzymatic-spectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestinewere taken for histological analysis .RESULTS One hour gut ischemia followed by reperfusion induction resulted in a significant elevation in plasma D (-) - lactate a nd LPS levels, and there was a significantcorrelation between the plasma D (-) - lactate and LPS (r = 0.719, P <0.05). The plasma concentrations of D (-) - lactate and LPS increased significantly at 6h postburn, and there D (-) - lactate and LPS levelselevated significantly at 2h after ANP, with a similarsignificant correlation between the two levels (r = 0.798, P <0.01). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propriawere observed in all groups. CONCLUSION The changes of plasma D (-) - lactate levels in systemic blood paralleled with LPS levels in the portal vein blood. The measurement of plasma D (-) - lactatelevel may be a useful marker to assess the intestinal in jury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage.