Journal
CARDIOVASCULAR RESEARCH
Volume 80, Issue 1, Pages 55-61Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvn162
Keywords
Ca(2+) waves; non-uniformity; delayed afterdepolarizations
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Funding
- Scientific Research Fund of Ministry of Education, Science, and Culture, Japan [12877102]
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Aims We examined whether non-uniform muscle contraction affects delayed afterdepolarizations (DADs) by dissociating Ca(2+) from myofilaments within the border zone (BZ) between contracting and stretched regions. Methods and results Force, sarcomere length (SL), membrane potential, and [Ca(2+)](i) dynamics were measured in 31 ventricular trabeculae from rat hearts. Non-uniform muscle contraction was produced by exposing a restricted region of muscle to a jet of solution containing 20 mmol/L 2,3-butanedione monoxime (BDM). DADs were induced by 7.5 s-2 Hz stimulus trains at an SL of 2.0 mu m (24 degrees C, [Ca(2+)](o) 2.0 mmol/L). The BDM jet enhanced DADs (n = 6, P < 0.05) and aftercontractions (n = 6, P < 0.05) with or without 100 mu mol/L streptomycin and occasionally elicited an action potential. A stretch pulse from an SL of 2.0 mu m to 2.1 or 2.2 mu m during the last stimulated twitch of the trains accelerated Ca(2+) waves in proportion to the increment of force by the stretch (P < 0.01) with or without streptomycin. In the presence of 1 mmol/L caffeine, rapid shortening of the muscle after the stretch pulse increased [Ca(2+)](i) within the BZ, whose amplitude correlated with the increment of force by the stretch (n = 15, P < 0.01). Conclusion These results suggest that non-uniform muscle contraction can enhance DADs by dissociating Ca(2+) from myofilaments within the BZ and thereby cause triggered arrhythmias.
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