Maintenance of cellular acidification in cyanide-treated hepatocytes results from inhibition of Na+/H+ exchange

Given that the sodiumpositive/hydrogenpositive exchanger is known to be a major component of pH regulation in normal hepatocytes, the effects of inhibition of mitochondrial respiration on intracellular pH (pHi) regulation and sodiumpositive/hydrogenpositive exchange were determined using cyanide plus fructose as a model of hypoxic acidosis. Inhibition of the exchange helped to maintain intracellular acidification, a condition that prolongs cell survival during hypoxia.