Intracellular sodium activity and Bretschneider's cardioplegia: Continuous measurement by ionselective microelectrodes at initial equilibration

Summary Intracellular sodium activity (a_Naⁱ), intracellular pH (pH_i) and membrane potential were directly and continuously measured in sheep cardiac Purkinje fibers using neutral carrier liquid membrane ionselective microelectrodes. Changing the superfusing medium from normal Tyrode's solution to the cardioplegic solution HTK according to Bretschneider (6) a depolarization from –73.7±7.2 mV to –55.0±9.5 mV (n=25), a decrease of a_Naⁱ from 9.1±1.9 mM to 4.0±1.4 mM (n=25) and an intracellular acidification from pH_i 7.18±0.06 to pH_i 7.01±0.06 (n=11, x±S.D.) occurred at 35°C. The decrease of intracellular sodium activity was not effected by replacement of K, Mg, or histidine by mannitol in the cardioplegic solution. Addition of 4 mM Ca somewhat enhanced a_Naⁱ decline. Inhibition of the sodium pump with the cardiac steroid dihydroouabain (10^–4 M) lowered the effect of HTK on intracellular sodium by approximately 35% (n=5). Sodium decline was also sensitive to equilibration temperature, giving a Q₁₀ of 1.54 for the initial decrease velocity (temperature range 20 to 35°C), which is less than that found by other investigators for pure sodium pump activity. It is suggested that although the electrochemical sodium gradient remains inward throughout, sodium may leave myocardial cells on induction of Bretschneider's cardioplegia because of a reduction of inward fluxes by simultaneously increasing sodium pump activity, thus increasing Na efflux. Na/Ca exchange is assumed to be of minor importance and the Na/H exchange may be involved. With respect to the clinical application of the low Na and nominally Ca-free cardioplegic solution HTK lowering of intracellular sodium activity is interpreted as a factor minimizing the risk of a calcium paradox on reperfusion with Ca at serum levels, as well as a possible mechanism preventing early development of cellular edema.Supported by the DFG, SFB 330 Organprotektion.Part of this work has already been published in abstract form (Pflüg. Arch. 1987: 408, R11) and comprises unpublished results of E. Krohn's thesis.The technical assistance of Mrs. U. Markmann and Mrs. E. Neumeyer is gratefully acknowledged.