Analysis of Cl- -HCO3(-) exchange during recovery from intracellular acidosis in cardiac Purkinje strands.

The possible role of a Cl- -HCO3(-) exchange mechanism in the recovery from intracellular acidosis of isolated cardiac Purkinje strands was investigated. Intracellular pH (pHi) was measured using double-barreled pH-sensitive microelectrodes. Acidifications were produced by withdrawing 20 meq NH+4 from the superfusate. Experiments were performed in normal CO2-HCO3(-)-buffered, in HCO3(-)free, and in Cl-free solutions and also in the presence of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), a blocker of Cl--HCO3(-) exchange. In the absence of external HCO3(-), the apparent rate of acid extrusion following induced acidification was only slightly decreased, but the observed effect does not necessarily imply the intervention of a Cl--HCO3(-) exchange mechanism. SITS had little effect on the response to acidification. In zero-Cl- solutions, recovery of pHi from acidosis was not impaired. These observations suggest that in Purkinje fibers, [Cl-]i-[HCO3(-)]o exchange plays no significant role in recovery from intracellular acidification. Moreover, additional evidence is presented in favor of a passive HCO3(-) efflux at steady-state pHi in the normal superfusate. The apparent membrane permeability to HCO-3 was estimated to be 3.2 X 10(-8) cm X s-1.