Original Research
Copyright ©The Author(s) 1997. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 1997; 3(4): 225-227
Published online Dec 15, 1997. doi: 10.3748/wjg.v3.i4.225
Plasma D (-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion
Yong-Ming Yao, Yan Yu, Ye Wu, Lian-Rong Lu, Zhi-Yong Sheng
Yong-Ming Yao, Yan Yu, Ye Wu, Lian-Rong Lu, Zhi-Yong Sheng, Department of Immunology, Burn Research Institute, Chinese PLA 304th Hospital, Beijing 100037, China
Ye Wu, Department of Surgery, Chinese PLA 223rd Hospital, Yanji 133000, Jilin Province, China
Yong-Ming Yao, was granted post doctor certification in 1995, Austria, Member of the New York Academy of Sciences, European Shock Society, and International Society for Burn Injuries, having 58 papers in Chinese and 51 articles in English published.
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Yong-Ming Yao, Department of Immunology, Burn Research Institute, Chinese PLA 304th Hospital, Beijing 100037, China
Telephone: +86-10-66813129-41394
Received: March 6, 1997
Revised: May 8, 1997
Accepted: June 23, 1997
Published online: December 15, 1997
Abstract

AIM: To observe the kinetics of D (-)-lactate alteration in both portal and systemic circulation systems, and its relationship with intestinal injury in rats subjected to acute intestinal ischemia-reperfusion.

METHODS: Anesthetized rats underwent a 75-min superior mesenteric artery occlusion followed by a 6-h reperfusion. Plasma D (-)-lactate levels were measured by an enzymatic spectrophotometric assay.

RESULTS: Intestinal ischemia for 75 min resulted in a significant elevation of D (-)-lactate levels in the portal vein, as compared with the baseline values (P < 0.05). Plasma D (-)-lactate levels had a tendency to further increase after reperfusion, up to 6 h. Similar alterations in D (-)-lactate were also found in systemic circulation, and there were no significant differences between the portal and systemic circulations at any time point. Moreover, the macropathological evaluation scores were significantly correlated to the portal D (-)-lactate levels in animals at various time points (r = 0.415, P < 0.01). In addition, there was a remarkable rise of endotoxin concentration within the portal vein at the end of the 75-min ischemic period (P < 0.05), reaching a peak at 2 h post-reperfusion.

CONCLUSION: Acute intestinal ischemia is associated with failure of the mucosal barrier resulting in increased plasma D (-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might further increase D (-)-lactate levels, which are correlated to the macropathological alterations. Plasma D (-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.

Keywords: D (-)lactate, Endotoxin, Intestinal injury, Reperfusion injury