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Artifactual contractions triggered by field stimulation of cardiomyocytes

¹Institute for Experimental Medical Research, and ²Department of Cardiology, Ullevaal University Hospital, and ³Center of Heart Failure Research, University of Oslo, N-0407 Oslo, Norway

Submitted 21 June 2004 ; accepted in final form 29 December 2004

Although cell shortening in patch-clamped cells (current-clamp mode) is triggered by an ordinary action potential, the trigger mechanism in field-stimulated cells is not so obvious. The contraction characteristics of the two methods differ, and we, therefore, examined the triggering sequence in field-stimulated cells. Isolated rat cardiomyocytes were plated on laminin-coated coverslips that were mounted on an inverted light microscope and superfused with HEPES-Tyrode buffer (pH 7.4; 37°C). The cells were stimulated to contract either by a 0.5-ms current injection (CC cells) through high-resistance electrodes or a 5-ms biphasic field-stimulation pulse (FS cells), and drugs were added to block sarcolemmal proteins involved in excitation-contraction coupling. Time to peak contraction (TTP) was significantly longer in FS cells and was not affected by the polarity or the length of the stimulus pulse. Tetrodotoxin (TTX; 20 µM) blocked cell shortening in CC cells but not in FS cells. Ni²⁺ (5 mM) blocked cell shortening in FS cells, whereas KB-R7943 (KB; 5 µM) had no effect either on cell shortening or TTP. In FS cells, nifedipine (Nif; 100 µM) and Cd²⁺ (300 µM) reduced fractional shortening by 34 and 63%, respectively, but only Cd²⁺ affected TTP (reduced by 48%). A combination of Nif and KB reduced cell shortening by 50%, whereas a combination of Cd²⁺ and KB almost abolished cell shortening. We conclude that field stimulation per se prolongs TTP and that cell shortening in FS cells is not dependent on Na⁺ current but is triggered by a combination of L-type Ca²⁺ current and reverse mode Na⁺/Ca²⁺ exchange.

excitation-contraction coupling; rat; L-type Ca²⁺ channel; Na⁺/Ca²⁺ exchanger

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