Effect of myocardial volume overload and heart failure on lactate transport into isolated cardiac myocytes

Abstract

The purpose of this study was to determine lactate transport kinetics in single isolated rat ventricular cardiac myocytes after 1) 8 wk of myocardial volume overload (MVO) and 2) congestive heart failure (CHF). Twenty male Sprague-Dawley rats were assigned to one of four groups: myocardial hypertrophy (MH), MH sham (MHS), CHF, or CHF sham (CHFS). A chronic MVO was induced in the MH and CHF groups by an infrarenal arteriovenous fistula. Postdeath heart and lung weights were significantly greater ( P < 0.05) for the MH and CHF groups compared with controls. Isolated cardiac myocytes were loaded with BCECF to determine intracellular pH (pHi) changes after the addition of lactate to the extracellular superfusate. Alterations in pHi with the addition of varied lactate concentrations were attenuated 72–89% by 5.0 mM α-cyano-4-hydroxycinnamate. Significant differences ( P < 0.05) were found in estimated maximal lactate transport rates between the experimental and sham groups (MH = 19.4 ± 1.1 nmol · μl−1 · min−1vs. MHS = 15.1 ± 1.1 nmol · μl−1 · min−1; CHF = 20.2 ± 2.0 nmol · μl−1 · min−1vs. CHFS = 14.0 ± 0.9 nmol · μl−1 · min−1). Western blot analysis confirmed a 270% increase in monocarboxylate symport protein 1 (MCT1) protein content in CHF compared with CHFS rats. The results of this study suggest that MH and CHF induced by MVO engender a greater maximal lactate transport capacity across the cardiac myocyte sarcolemma along with an increase in MCT1 protein content. These alterations would likely benefit the cell by attenuating intracellular acidification during a period of increased myocardial load.