Abstract

Ion flux studies were performed on Langendorff-perfused rat hearts using 87Rb, 7Li and 23Na NMR at 36, 20 and 10°C, and at constant extracellular pH (7.40). Using 31P NMR, the intracellular pH was estimated and the high energy phosphate content monitored. Compared to 36°C ( k=0.044±0.015 min −1), our measurements showed incomplete Rb + efflux with a dramatically (5-fold) increased rate constant, k, at 20°C, k=0.238±0.080 min −1. 5 μM glibenclamide, a K ATP-channel inhibitor, completely depressed the hypothermia-activated Rb + efflux at this temperature ( k=0.052±0.018 min −1). 7Li NMR efflux studies on KCl-arrested hearts at 20°C also showed an increase (3-fold) in efflux rate constant: k=0.090±0.003 min −1 relative to its value at 36°C. At 10°C, both Rb + and Li + showed efflux rate constants similar to those observed at 36°C, k=0.071±0.016 min −1 and k=0.050±0.005 min −1, respectively, and the washout was complete. 31P NMR at 36, 20 and 10°C indicated cytosolic alkalinization at pH values of 7.05, 7.21 and 7.40, respectively. The ion transport data could be interpreted in terms of a myocyte model allowing for temperature-dependent changes in transport coefficients. The incomplete efflux of Rb + at 20°C may indicate the existence of a mitochondrial Rb +-pool with a very low Rb + permeability for efflux. These findings correlate with previously observed membrane phase transitions in these systems.

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