Myocardial CO2 buffering: role of transmembrane transport of H+ or HCO3-ions.
Isolated rabbit hearts were perfused with rabbit red cells suspended in Ringer solution. A small volume of perfusate was recirculated for 10 min at Pco2 of 33.4 +/- 0.9 or 150.8 +/- 7.5 mmHg. Hypercapnia resulted in an increase in perfusate HCO3- concentration that was smaller than that observed when isolated perfusate was equilibrated in vitro with the same CO2 tensions (delta HCO-3e = 1.6 mM, P less than 0.01). This difference is consistent with a net movement of HCO3- into or H+ out of the mycardial cell, and cannot be accounted for by dilution of HCO3- in the myocardial interstitium. Recirculation of perfusate through the coronary circulation at normal Pco2 for two consecutive 10-min periods was not followed by changes in perfusate HCO3- concentration. A high degree of correlation (r = 0.81) was observed between intracellular HCO-3e concentration and the corresponding delta HCO-3e in individual experiments. The results suggest that transmembrane  exchange of H+ or HCO3- is a buffer mechanism for CO2 in the myocardial cell.
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D001692:Biological Transport; D002245:Carbon Dioxide / Q000378:metabolism*; D002463:Cell Membrane Permeability; D006859:Hydrogen / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D011817:Rabbits
D001639:Bicarbonates; D002245:Carbon Dioxide; D006859:Hydrogen