Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats

AIM To explore the kinetic changes in plasma D (-)lactate and lipopolysacch aride ( 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: 10 gut ischemia/ reperfusion o btained by one hour of superior mesenteric artery occlusion followed by rep erfusion; 2 severe burn injury created by 30% of total body surface area ( TBSA) full-thickness scald burn; and 3 ANP induced by continuous inverse in fusion of sodium taurocholate and trypsin into main pancreatic duct. Plasm a levels of D(-)-lactate in systemic circulation and LPS in portal circulat ion were measured by enzymatic-spectrophotometric method and limulus ameboc yte lysate (LAL) test kit, respectively. Tissue samples of intestine were t aken for histological analysis. RESULTS One hour gut ischemia followed by reperfusion injuries resulted in a significant elevation in plasma D( -)lactate and LPS levels, and there wa s a significant correlation between the plasma D(-)-lactate and LPS (r = 0. 719, P < 0.05). The plasma concentrations of D (-) lactate and LPS increase d significantly at 6 h postburn, and there was also a remarkable correlatio n between them (r = 0.877, P < 0.01). D (-)-lactate and LPS levels elevated significantly at 2 h after ANP, with a similar significant correlation bet ween the two levels ( r = 0.798, P < 0.01). The desquamation of intestine v illi and infiltration of inflammatory cells in the lamina propria were obse rved in all groups. CONCLUSION The changes of plasma D(-)-lactate levels in systemic blood para lleled with LPS levels in the portal vein blood. The measurement of plasma D (-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia follo wing severe injuries in early stage.