AIM To explore the kinetic changes in plasma D (-)lactate and lipopolysaccharide ( 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:gut ischemia/reperfusion obtained by one hour of superior severe burn injury created by 30% of total body surface induced by continuous inverse infusion of sodium taurocholate and trypsin into main pancreatic duct.Plasma levels of D( - )-lactate in systemic circulation and LPS in portal circulation were measured by enzymaticspectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestine were taken 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 was a significant correlation between the plasma D( - )-lactate and LPS (r =0.719, P＜0.05). The plasma concentrations of D(-)lactate and LPS increased significantly at 6 h postburn,and there was also a remarkable correlation 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 between the two levels (r-0.798,P ＜ 0.01 ). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propria were 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 (-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage.
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