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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.

Because central venous O2 saturation (superior vena cava, ScvO2) can be monitored with less patient risk than mixed venous O2 saturation (pulmonary artery, SvO2), we examined the correlations between SvO2 and ScvO2 over a broad range of cardiorespiratory conditions, including hypoxia, hemorrhage, and resuscitation in anesthetized dogs. The correlation coefficient (r) between SvO2 and ScvO2 in 179 simultaneously drawn blood samples from 22 dogs was 0.97. In another nine dogs, the two sites were continuously and simultaneously monitored with fiberoptic catheters; r was 0.96 with a mean difference of 3.7 +/- 2.9 percent (SD) saturation. In each dog the changes in ScvO2 closely paralleled the changes in SvO2. Although absolute values of ScvO2 are not sufficiently identical to SvO2 to calculate O2 uptake or pulmonary shunt precisely, close tracking of changes in the two sites across a wide range of hemodynamic conditions warrant further consideration of ScvO2 for patient monitoring of trends in O2 supply/demand.

Several reports state that oxygen uptake changed in direct correlation with changes in total oxygen delivery to the tissues in the adult respiratory distress syndrome (ARDS). Oxygen uptake appeared to be limited by oxygen delivery even at normally adequate levels so that uptake was abnormally dependent on supply. These reports are discussed with respect to whether or not such a result could have been due to errors in measurement or to mathematical coupling by relating two quantities that shared a common variable. Having rejected that proposition, animal experiments are cited in which abnormal oxygen supply dependency was produced by microembolization. The accompanying loss of reactive hyperemia and inability to extract oxygen were consistent with a progressive loss of recruitable capillaries. Evidence is presented that the potential for embolization in ARDS is greatly enhanced by activation of the complement and arachidonic acid cascades as well as by the xanthine oxidase system. The resultant use of molecular oxygen by non-ATP producing oxidase systems might also account for the increase of supply dependent oxygen demand in ARDS.