Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats

Abstract

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: gut ischemia/reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and 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 enzymaticspectrophotometric 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.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.Subject headings gut/injury; ischemia reperfusion/ blood; burn/blood; acute necrotizing pancreatitis/blood; D ( -)-lactate/blood; lipopolysaccharide/blood; intestinal permeability Sun XQ, Fu XB, Zhang R, Lü Y, Deng Q, Jiang XG, Sheng ZY. Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats. World J Gastroenterol, 2001;7(4):555-558

Differential effect of imipenem treatment on injury caused by cecal ligation and puncture in wild-type and NK cell-deficient β2-microgloblin knockout mice

“…It has been postulated that endotoxin translocation is a major stimulus for postischemic inflammation. Some reports showed a clear correlation between plasma endotoxin concentrations, lactate production, and proinflammatory cytokine re- lease in models of postburn and hemorrhagic shock (22). NK cells are known to facilitate endotoxin-induced shock by producing interferon (IFN)-␥ (31).…”

“…Hypothermia and severe metabolic acidosis are predictors of mortality in mice after CLP (18,19). Metabolic acidosis is a surrogate marker of tissue hypoperfusion and is commonly seen during gut ischemia and in shock states (22). The presence of severe metabolic acidosis indicates that a state of tissue hypoperfusion exists in wild-type mice after CLP.…”

An experimental evaluation of the lactate concentration following mesenteric ischemia

“…Since Sun et al reported that the D-lactate level did not increase in the peripheral vessel blood at an early phase in a mesenteric ischemia model using rats and that the reperfusion of the SMA was necessary to make an early diagnosis of mesenteric ischemia, it might thus be diffi cult to diagnose mesenteric ischemia at an early phase by peripheral blood tests. 12,13 However, when we talk about mesenteric ischemia secondary to aortic dissection, there is still a possibility of making an early diagnosis using blood tests of the hepatic vein because our animal model does not present mesenteric ischemia secondary to aortic dissection, which affects not only SMA but also many collateral sources into the intestines.…”

Increased Circulating D-Lactate Levels Predict Risk of Mortality After Hemorrhage and Surgical Trauma in Baboons

“…Many authors have already shown a significant increase of plasma D-lactate levels in different experimental and clinical studies such as in acute mesenteric ischemia, bowel obstruction, acute abdomen, peritonitis, necrotizing pancreatitis, and in a rodent model of hemorrhagic shock (12,26,31,32,37). Considering the gut as possible cause of MOF, we hypothesized that D-lactate measurement could predict mortality following hemorrhage and trauma.…”