[Intestinal mucosa injury during experimental endotoxin-induced shock].

To ascertain tissue oxygenation during conversion from hypo to hyperdynamic state with vascular volume expansion, venous outflow from a segment of ileum was isolated in anesthetized and pump-ventilated endotoxic dogs to measure gut oxygen uptake (VO2), lactate metabolism, intramucosal PCO2 and tissue PO2 (PtiO2). Tissue PO2 was measured by multipoint surface Mehrdraht Dortmund Oberfläche electrodes placed on mucosal and serosal surfaces of gut. Six dogs were infused with 2 mg.kg-1 E. coli lipopolysaccharide (LPS) in one hour followed by a two hour 0.5 mL.kg-1.min-1 dextran infusion. Two dogs were used as controls and received dextran infusion in order to assess time and hemodilution-dependent effects. LPS infusion resulted in an hypodynamic sepsis with supply limited VO2, increased arterial lactate and increased lactate output by gut. Resuscitation resulted in an hyperdynamic sepsis with improvement of whole-body VO2. In the gut, VO2 remained low and intramucosal PCO2 as well as lactate output remained high, despite increased flow. Gut PtiO2 results suggested blood flow maldistribution with tissue hypoxia in the mucosa despite increased total flow to the gut. Gut VO2, lactate flux, intramucosal PCO2, and tissue PO2 were consistent with regulatory responses that shut down mucosal perfusion and oxygenation in spite of increased blood flow to gut.