Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by PCO2

Rozenfeld, Ranna A., Michael K. Dishart, Tor IngeTønnessen, and Robert Schlichtig. Methods for detecting localintestinal ischemic anaerobic metabolic acidosis byPCO₂. J. Appl. Physiol. 81(4): 1834-1842, 1996.Gut ischemia isoften assessed by computing an imaginary tissue interstitial pH fromarterial plasma HCO₃ and thePCO₂ in a saline-filled balloontonometer after equilibration with tissuePCO₂ (Pti_CO2).Pti_CO2 mayalternatively be assumed equal to venous PCO₂(Pv_CO2) in that region of gut. The ideais that as blood flow decreases, gutPti_CO2 andPv_CO2 will increase to the maximumaerobic value, i.e., maximum respiratoryPv_CO2(Pv_CO2 rmax). Above a "critical" anaerobic threshold, lactate(La) generation, bytitration of tissue HCO₃, should raisePti_CO2abovePv_CO2 rmax.During progressive selective whole intestinal flow reduction insix pentobarbital-anesthetized pigs, we usedPCO₂ electrodes to test thehypotheses that criticalPti_CO2is achieved earlier in mucosa than in serosa and thatPv_CO2 rmax,computed using an in vitro model, predicts criticalPti_CO2. Wedefined criticalPti_CO2 as theinflection ofPti_CO2-Pv_CO2vs. O₂ delivery(O₂)plots. CriticalO₂for O₂ uptake was 12.55 ± 2 ml ^· kg^{1 ·} min¹.Critical Pti_CO2 for mucosaand serosa was achieved at similar whole intestineO₂(13.90 ± 5 and 13.36 ± 5 ml ^· kg^{1 ·} min¹,P = NS). CriticalPti_CO2 (129 ± 24 and 96 ± 21 Torr) exceeded Pv_CO2 rmax(62 ± 3 Torr). During ischemia,La excretion into portalvenous blood was matched by K⁺excretion, causing Pv_CO2 to increaseonly slightly, despitePti_CO2 risingto 380 ± 46 (mucosa) and 280 ± 38 (serosa) Torr. These resultssuggest that mucosa and serosa become dysoxic simultaneously, thatischemic dysoxic gut is essentially unperfused, and that in vitropredictedPv_CO2 rmaxunderestimates criticalPti_CO2.