Postcapillary pH disequilibrium after gas exchange in isolated perfused liver

pH equilibration after gas exchange in a systemic vascular bed was investigated using an isolated guinea pig liver preparation perfused with a blood-free Krebs-Ringer-bicarbonate solution. Effluent perfusate was withdrawn into a stopped-flow apparatus in which pH and temperature were continuously monitored. A decrease in pH of the perfusate after exit from the liver was observed. Addition of acetazolamide to inflowing perfusate had little effect on this fall in effluent fluid pH, while the addition of carbonic anhydrase completely abolished the decrease in pH. These results suggest that: 1) after the addition of metabolically produced CO2, the reaction CO2 leads to H2CO3 leads to H+ + HCO3- in the perfusate did not reach equilibrium during passage through the liver; 2) acetazolamide had little effect on the magnitude of the pH disequilibrium; and 3) carbonic anhydrase accelerated the reaction to equilibrium. We conclude that little or no catalysis of the conversion of perfusate CO2 to H2CO3 takes place within the hepatic circulation and that the presence of slow postcapillary blood pH changes in vivo may be dependent on the specific species and organ vascular bed from which the blood exited after participating in gas exchange.