Metabolic component of intestinal Pco 2during dysoxia

The adequacy of intestinal perfusion during shock and resuscitation might be estimated from intestinal tissue acid-base balance. We examined this idea from the perspective of conventional blood acid-base physicochemistry. As the O2 supply diminishes with failing blood flow, tissue acid-base changes are first “respiratory,” with CO2 coming from combustion of fuel and stagnating in the decreasing blood flow. When the O2supply decreases to critical, the changes become “metabolic” due to lactic acid. In blood, the respiratory vs. metabolic distinction is conventionally made using the buffer base principle, in which buffer base is the sum of HCO3 − and noncarbonate buffer anion (A−). During purely respiratory acidosis, buffer base stays constant because HCO3 − cannot buffer its own progenitor, carbonic acid, so that the rise of HCO3 − equals the fall of A−. During anaerobic “metabolism,” however, lactate's H+ is buffered by both A− and HCO3 −, causing buffer base to decrease. We quantified the partitioning of lactate's H+ between HCO3 − and A−buffer in anoxic intestine by compressing intestinal segments of anesthetized swine into a steel pipe and measuring Pco 2 and lactate at 5- to 10-min intervals. Their rises followed first-order kinetics, yielding k = 0.031 min−1 and half time = ∼22 min. Pco 2 vs. lactate relations were linear. Over 3 h, lactate increased by 31 ± 3 mmol/l tissue fluid (mM) and Pco 2 by ∼17 mM, meaning that one-half of lactate's H+ was buffered by tissue HCO3 − and one-half by A−. The data were consistent with a lumped p K a value near 6.1 and total A− concentration of ∼30 mmol/kg. We conclude that the respiratory vs. metabolic distinction could be made in tissue by estimating tissue buffer base from measured pH and Pco 2.