Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats.
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.
Sun
X Q
XQ
Burn Institute, Trauma Center, 304th Hospital, Beijing 100037, China. fu xb@cgw.net.cn
Fu
X B
XB
Zhang
R
R
Lu
Y
Y
Deng
Q
Q
Jiang
X G
XG
Sheng
Z Y
ZY
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
D015415:Biomarkers; D008070:Lipopolysaccharides; D019344:Lactic Acid