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Myocardial intracellular pH regulation during chloride depletion.

The possible role of a HCO-3/Cl- transmembrane exchange as a mechanism of alkalinization in the myocardial cell was studied in isolated rabbit hearts perfused with Ringer solution. Cl- depletion was produced by replacing Cl- of the perfusate by SO2(-4) or glucuronate. Intracellular pH (pHi) was calculated both in Cl--free and Cl--containing hearts from the distribution of 14C-labeled 5',5'-dimethyloxazolidine-2,4-dione. Acid-base alterations were produced by changing perfusate HCO-3 concentration and/or CO2 partial pressure (PCO2). Depletion of Cl- resulted in an increase in pHi for any given level of extracellular pH. Increasing PCO2 at constant perfusate HCO-3 resulted in changes in pHi and cell HCO-3 (HCO-3i) that were similar in both Cl--free and Cl--containing hearts. Increasing perfusate HCO-3 at constant PCO2 resulted in increases in pHi and HCO-3i in both Cl--free and Cl--containing preparations. When the increases in HCO-3i secondary to an increase in extracellular HCO-3 were plotted as a function of the initial HCO-3i, a significant negative correlation was observed, suggesting that the elevation of HCO-3i was influenced by the initial HCo-3i and not by the presence or absence of Cl-. It is concluded that even though HCO-3 may enter the myocardial cells in exchange for Cl- during Cl-depletion, lack of Cl- does not alter the ability of the myocardial cell to regulate its pHi. This argues against a HCO-3/Cl- exchange as a mechanism of regulation of myocardial pHi.