title: Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats.
abstract: OBJECTIVE
  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: (1)gut ischemia/reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; (2)severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and (3)ANP 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 enzymatic-spectrophotometric 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 6h postburn, and there was also a remarkable correlation between them (r=0.877 P<0.01). D(-)-lactate and LPS levels elevated significantly at 2h 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Burn Institute, Trauma Center, 304th Hospital, Beijing 100037, China. fu xb@cgw.net.cn
authors.forename: X Q
authors.initials: XQ
authors.lastname: Sun
authors.forename: X B
authors.initials: XB
authors.lastname: Fu
authors.forename: R
authors.initials: R
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Lu
authors.forename: Q
authors.initials: Q
authors.lastname: Deng
authors.forename: X G
authors.initials: XG
authors.lastname: Jiang
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Sheng
mesh_terms: D000818:Animals; D015415:Biomarkers; D002056:Burns / Q000097:blood*; D004195:Disease Models, Animal; D007422:Intestines / Q000473:pathology*; D007511:Ischemia / Q000097:blood* / Q000473:pathology; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood*; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood*; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion
chemical_list: D015415:Biomarkers; D008070:Lipopolysaccharides; D019344:Lactic Acid