Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by PCO₂

Gut ischemia is often assessed by computing an imaginary tissue interstitial pH from arterial plasma HCO₃ and the PCO₂ in a saline-filled balloon tonometer after equilibration with tissue PCO₂ (Pti(CO₂). Pti(CO₂) may alternatively be assumed equal to venous PCO₂ (Pv(CO₂)) in that region of gut. The idea is that as blood flow decreases, gut Pti(CO₂), and Pv(CO₂), will increase to the maximum aerobic value, i.e., maximum respiratory Pv(CO₂) (Pv(CO₂rmax)). Above a 'critical' anaerobic threshold, lactate (La^-) generation, by titration of tissue HCO₃, should raise Pti(CO₂) above Pv(CO₂ rmax). During progressive selective whole intestinal flow reduction in six pentobarbital-anesthetized pigs, we used PCO₂ electrodes to test the hypotheses that critical Pti(CO₂) is achieved earlier in mucosa than in serosa and that Pv(CO₂ rmax), computed using an in vitro model, predicts critical Pti(CO₂). We defined critical Pti(CO₂) as the inflection of Pt(CO₂)-Pv(CO₂) vs. O₂ delivery (Q̇O₂) plots. Critical Q̇O₂ for O₂ uptake was 12.55 ± 2 ml · kg^-1 · min^-1. Critical Pti(CO₂)) for mucosa and serosa was achieved at similar whole intestine Q̇O₂ (13.90 ± 5 and 13.36 ± 5 ml · kg^-1 · min^-1, P = NS). Critical Pti(CO₂) (129 ± 24 and 96 ± 21 Torr) exceeded Pv(CO₂rmax) (62 ± 3 Torr). During ischemia, La^- excretion into portal venous blood was matched by K⁺ excretion, causing Pv(CO₂) to increase only slightly, despite Pti(CO₂) rising to 380 ± 46 (mucosa) and 280 ± 38 (serosa) Torr. These results suggest that mucosa and serosa become dysoxic simultaneously, that ischemic dysoxic gut is essentially unperfused, and that in vitro predicted Pv(CO₂rmax) underestimates critical Pti(CO₂).