High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts

doi:10.1016/j.ejheart.2006.01.013

European Journal of Heart Failure 2006 8(7):673-680; doi:10.1016/j.ejheart.2006.01.013

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High intracellular Na⁺ preserves myocardial function at low heart rates in isolated myocardium from failing hearts

Wolfgang Schillinger^a^,*^,1, Nils Teucher^a^,1, Claus Christians^a, Michael Kohlhaas^a, Samuel Sossalla^a, Phuc Van Nguyen^a, Albrecht G. Schmidt^a, Ortwin Schunck^b, Klaus Nebendahl^b, Lars S. Maier^a, Oliver Zeitz^a^,2 and Gerd Hasenfuss^a

^a Georg-August-Universität Göttingen, Herzzentrum, Kardiologie und Pneumologie, Robert-Koch-Str. 40, 37099 Göttingen, Germany
^b Georg-August Universität Göttingen, Zentrale Tierexperimentelle Einrichtung, Göttingen, Germany

^* Corresponding author. Tel.: +49 551 39 6349; fax: +49 551 39 9804. E-mail address: schiwolf{at}med.uni-goettingen.de (W. Schillinger).

Abstract

We investigated the hypothesis that increased intracellular[Na⁺]_i in heart failure contributes to preservation of SR Ca²⁺load which may become particularly evident at slow heart rates.

[Na⁺]_i in SBFI-loaded myocytes from rabbits with pacing-inducedheart failure (PHF) was significantly higher at each frequencyas compared to Sham-operated animals. Furthermore, PHF rabbitsdemonstrated reduced SR Ca²⁺-ATPase protein levels (–37%, p < 0.04) but unchanged Na⁺/Ca²⁺ exchanger protein levels.At 0.25 Hz, isometric force was similar in cardiac trabeculaefrom PHF rabbits as compared to control (PHF, 3.6±1.3;Sham, 4.4 ± 0.6 mN/mm²). Rapid cooling contractures (RCCs)were unchanged indicating preserved SR Ca²⁺ load at this frequency.In Sham, isometric twitch force increased with rising frequenciesto 29.0 + 2.8 mN/mm² at 3.0 Hz (p < 0.05) as compared to0.25 Hz. RCCs showed a parallel increase by 186 ± 47%(p < 0.01). In PHF, frequency-dependent increase in force(15.8 ± 4.7 mN/mm² at 3.0 Hz) and RCCs (increase by 70± 40%) were significantly blunted.

Thus, in PHF in rabbits SR Ca²⁺ load is preserved at low frequenciesdespite decreased SR Ca²⁺-ATPase expression. This may resultfrom [Na⁺]_i-dependent changes in Na⁺/Ca²⁺ exchanger activity.

Key Words: Dilated cardiomyopathy • Heart failure • Force–frequency relationship • Sodium • Animal model

Received July 21, 2005; Revised October 28, 2005; Accepted January 25, 2006

¹ Both authors contributed equally to this work.

² Current address: Universitätsklinikum Hamburg-Eppendorf,Klinik und Poliklinik für Augenheilkunde, Hamburg, Germany.

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