Abstract
Intracellular pH (pHi) in sheep cardiac Purkinje fibres is controlled by sarcolemmal Na+/H+ and Cl-/HCO3- exchange. At normal pHo (7.4), Na+/H+ exchange mediates an acid efflux whenever pHi falls and Cl-/HCO3- exchange mediates an equivalent acid influx in response to a rise in pHi. Intracellular pH is also influenced by Ca2+i, which can activate force development leading to the anaerobic production of lactic acid. This is evident after an increase in stimulation rate which reversibly reduces both pHi and extracellular surface pH (pHs). Rate-dependent pHi changes are inhibited following inhibition of glycolysis, indicating that they are caused by accumulation of lactic acid. In some cases, the efflux of lactic acid may provide a faster method for recovery of pHi from a metabolic acidosis than that provided by Na+/H+ exchange. Finally, direct pHi measurement in isolated mammalian ventricular myocytes suggests that the intrinsic intracellular buffering power (beta) of ventricular tissue may be considerably lower than previously believed. An accurate knowledge of beta is essential for calculating net membrane fluxes of acid equivalents from changes in pHi.
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