Original Research
Copyright ©The Author(s) 2001. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 15, 2001; 7(4): 555-558
Published online Aug 15, 2001. doi: 10.3748/wjg.v7.i4.555
Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats
Xiao-Qing Sun, Xiao-Bing Fu, Rong-Zhang, Yi Lü, Qun Deng, Xiao-Guo Jiang, Zhi-Yong Sheng
Xiao-Qing Sun, Xiao-Bing Fu, Rong-Zhang, Yi Lü, Xiao-Guo Jiang, Zhi-Yong Sheng, Burn Institute, 304th Hospital, Beijing 100037, China
Qun Deng, Department of General Surgery, Chinese PLA 304 Hospital, Beijing 100037, China
Author contributions: All authors contributed equally to the work.
Supported by the Fund for National Outstanding Young Researchers of China, No. 39525024
Correspondence to: Dr. Xiao-Qing Sun, Trauma Center, 304th Hospital, Beijing 100037, China. fuxb@cgw.net.cn
Telephone: 0086-10-66867391 Fax: 0086-10-68429998
Received: April 6, 2001
Revised: May 5, 2001
Accepted: May 12, 2001
Published online: August 15, 2001

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: 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 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.

Keywords: gut/injury, ischemia reperfusion/blood, burn/blood, acute necrotizing pancreatitis/blood, D(-)-lactate/blood, lipopolysaccharide/blood, intestinal permeability