METHODS FOR DETECTING FOCAL INTESTINAL ISCHEMIC ANAEROBIC METABOLIC-ACIDOSIS BY PCO2

Gut ischemia is often assessed by computing an imaginary tissue inters titial pH from arterial plasma HCO3- and PCO2 in a saline-filled ballo on tonometer after equilibration with tissue PCO2 (Pti(CO2)). Pti(CO2) may alternatively be assumed equal to venous PCO2 (Pv(CO2)) in that r egion of gut. The idea is that as blood flow decreases, gut Pti(CO2) a nd Pv(CO2) will increase to the maximum aerobic value, i.e., maximum r espiratory Pv(CO2) (Pv(CO2rmax)). Above a ''critical'' anaerobic thres hold, lactate (La-) generation, by titration of tissue HCO3-, should r aise Pti(CO2) above Pv(CO2rmax). During progressive selective whole in testinal flow reduction in six pentobarbital-anesthetized pigs, we use d PCO2 electrodes to test the hypotheses that critical Pti(CO2) is ach ieved earlier in mucosa than in serosa and that Pv(CO2rmax), computed using an in vitro model, predicts critical Pti(CO2). We defined critic al Pti(CO2) as the inflection of Pti(CO2)-Pv(CO2) vs. O-2 delivery (QO (2)) plots. Critical QO(2) for O-2 uptake was 12.55 +/- 2 ml . kg(-1). min(-1). Critical Pti(CO2) for mucosa and serosa was achieved at simi lar whole intestine QO(2) (13.90 +/- 5 and 13.36 +/- 5 ml . kg(-1). mi n(-1), P = NS). Critical Pti(CO2) (129 +/- 24 and 96 +/- 21 Torr) exce eded Pv(CO2rmax) (62 +/- 3 Torr). During ischemia, La- excretion into portal venous blood was matched by K+ excretion, causing Pv(CO2) to in crease only slightly, despite Pti(CO2) rising to 380 +/- 46 (mucosa) a nd 280 +/- 38 (serosa) Torr. These results suggest that mucosa and ser osa become dysoxic simultaneously, that ischemic dysoxic gut is essent ially unperfused, and that in vitro predicted Pv(CO2rmax) underestimat es critical Pti(CO2).