Y Yao1, Z Sheng, Y Wu. 1. Burn Institute, 304th Hospital of People's Liberation Army, Beijing.
Abstract
OBJECTIVE: To determine the kinetics of plasma D(-)-lactate levels in both portal and systemic circulations, and to examine whether elevated plasma D(-)-lactate would correlate to intestinal injury in rats subjected to acute intestinal ischemia-reperfusion. METHODS: Anesthetized rats underwent 75 minutes of superior mesenteric artery occlusion followed by 6 hours of reperfusion. Plasma D(-)-lactate levels were measured by an enzymatic spectrophotometric assay. RESULTS: It showed that intestinal ischemia for 75 minutes resulted in a significant elevation in D(-)-lactate levels in portal vein blood compared to baseline values (P < 0.05). Plasma D(-)-lactate levels had a tendency to further increase after reperfusion up to 6 hours. Similar alterations in D(-)-lactate were also found in systemic circulation, there were no significant differences between the portal and systemic circulation at any time point. Moreover, the histopathological 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, a remarkable rise of endotoxin concentration within portal vein was already found at the end of 75-minute ischemia (P < 0.05), reaching a peak at 2 hours post-reperfusion. CONCLUSION: These data suggest that acute intestinal ischemia is associated with failure of mucosal barrier resulting in increased plasma D(-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might cause further increase in D(-)-lactate levels, which correlated to the histopathological alterations. Plasma D(-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.
OBJECTIVE: To determine the kinetics of plasma D(-)-lactate levels in both portal and systemic circulations, and to examine whether elevated plasma D(-)-lactate would correlate to intestinal injury in rats subjected to acute intestinal ischemia-reperfusion. METHODS: Anesthetized rats underwent 75 minutes of superior mesenteric artery occlusion followed by 6 hours of reperfusion. Plasma D(-)-lactate levels were measured by an enzymatic spectrophotometric assay. RESULTS: It showed that intestinal ischemia for 75 minutes resulted in a significant elevation in D(-)-lactate levels in portal vein blood compared to baseline values (P < 0.05). Plasma D(-)-lactate levels had a tendency to further increase after reperfusion up to 6 hours. Similar alterations in D(-)-lactate were also found in systemic circulation, there were no significant differences between the portal and systemic circulation at any time point. Moreover, the histopathological 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, a remarkable rise of endotoxin concentration within portal vein was already found at the end of 75-minute ischemia (P < 0.05), reaching a peak at 2 hours post-reperfusion. CONCLUSION: These data suggest that acute intestinal ischemia is associated with failure of mucosal barrier resulting in increased plasma D(-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might cause further increase in D(-)-lactate levels, which correlated to the histopathological alterations. Plasma D(-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.