We tested the hypothesis that endotoxin increases the heterogeneity of gut capillary transit times and impairs oxygen extraction. The gut critical oxygen extraction ratio was determined by measuring multiple oxygen delivery-consumption points during progressive phlebotomy in eight control and eight endotoxin-infused anesthetized pigs. In multiple 1- to 2-g samples of small bowel, we measured blood volume (radiolabeled red blood cells) and flow (radiolabeled 15-microns microspheres) before and after critical oxygen extraction. Red blood cell transit time (= volume/flow) multiplied by morphologically determined capillary/total blood volume gave capillary transit time. During hemorrhage, capillary/total blood volume did not change in the endotoxin group (0.5 +/- 4.5%) but increased in the control group (17.6 +/- 2.5%; P < 0.05) due to a decrease in total gut blood volume. Flow decreased significantly in the endotoxin group (36 +/- 10%; P < 0.05) but not in the control group (12 +/- 10%). Capillary transit-time heterogeneity increased in the endotoxin group (12.3 +/- 4.9%) compared with the control group (-5.8 +/- 7.4%; P < 0.05), predicting a critical oxygen extraction ratio 0.14 lower in the endotoxin group than in the control group (K. R. Walley. J. Appl. Physiol. 81: 885-894, 1996). This matches the measured difference (endotoxin group, 0.60 +/- 0.04; control group, 0.74 +/- 0.03; P < 0.05). Increased heterogeneity of capillary transit times may be an important cause of impaired oxygen extraction.
Gastric tonometer PCO2 measurement may help identify gut ischemia in critically ill patients but is frequently associated with large measurement errors. We tested the hypothesis that small bowel tonometer PCO2 measurement yields more accurate information. In 10 anesthetized, mechanically ventilated pigs subject to progressive hemorrhage, we measured gut oxygen delivery and consumption. We also measured tonometer PCO2 minus arterial PCO2 (DeltaPCO2) and calculated the corresponding intracellular pH from tonometers placed in the stomach and jejunum. We found that the correlation coefficient (r2) for biphasic gut oxygen delivery-DeltaPCO2 relationships was 0.29 +/- 0.52 for the gastric tonometer vs. 0.76 +/- 0.25 for the small bowel tonometer (P < 0.05). In addition, the critical gastric tonometer DeltaPCO2 was excessively high and variable (62.9 +/- 39.6) compared with the critical small bowel tonometer DeltaPCO2 (17.0 +/- 15.0, P < 0.01). Small bowel tonometer PCO2 was closely correlated with superior mesenteric vein PCO2 (r2 = 0.81, P < 0.001), whereas gastric tonometer PCO2 was not (r2 = -0.13, P = not significant). We conclude that measurement of gastric tonometer PCO2 yields excessively noisy and inaccurate data on the onset of gut anaerobic metabolism in hemorrhagic shock. Small bowel tonometer PCO2 is less noisy and, as a result, is superior in detecting gut hypoperfusion and the onset of anaerobic metabolism.
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