INTESTINAL MUCOSAL INJURY DURING EXPERIME NTAL ENDOTOXIC-SHOCK

To ascertain tissue oxygenation during conversion from hypo to hyperdy namic state with vascular volume expansion, venous outflow from a segm ent of ileum was isolated in anesthetized and pump-ventilated endotoxi c dogs to measure gut oxygen uptake (Vo(2)), lactate metabolism, intra mucosal Pco(2) and tissue Po-2 (Ptio(2)). Tissue Po-2 was measured by multipoint surface Mehrdraht Dortmund Oberflache electrodes placed on mucosal and serosal surfaces of gut. Six dogs were infused with 2 mg.k g(-1) E. coli lipopolysaccharide (LPS) in one hour followed by a two h our 0.5 mL.kg(-1).min(-1) dextran infusion. Two dogs were used as cont rols and received dextran infusion in order to assess time and hemodil ution-dependent effects. LPS infusion resulted in an hypodynamic sepsi s with supply limited Vo(2), increased arterial lactate and increased lactate output by gut. Resuscitation resulted in an hyperdynamic sepsi s with improvement of whole-body Vo(2). In the gut, Vo(2) remained low and intramucosal Pco(2) as well as lactate output remained high, desp ite increased now. Gut Ptio(2) results suggested blood flow maldistrib ution with tissue hypoxia in the mucosa despite increased total now to the gut. Gut Vo(2), lactate flux, intramucosal Pco(2), and tissue Po- 2 were consistent with regulatory responses that shut down mucosal per fusion and oxygenation in spite of increased blood flow to gut.