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Am J Physiol Heart Circ Physiol 274: H266-H276, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 1, H266-H276, January 1998

Ca2+ waves during triggered propagated contractions in intact trabeculae

Masahito Miura1, Penelope A. Boyden2, and Henk E. D. J. Ter Keurs1

1 Department of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1; and 2 Department of Pharmacology, Columbia College of Physicians and Surgeons, New York, New York 10032

Triggered propagated contractions (TPCs) starting from damaged regions travel along multicellular cardiac muscle preparations. We have reported that octanol (100 µM) inhibits TPCs. The inhibitory effect of octanol on propagation of TPCs could be due to an effect of octanol on Ca2+-induced Ca2+ release (CICR) mediated by Ca2+ diffusion inside the single cell or on the diffusion of Ca2+ from cell to cell via gap junctions (GJs). Therefore, we studied the regional changes in intracellular Ca2+ concentration ([Ca2+]i) during TPCs and the effect of octanol on the permeability of gap junctions (PGJ) in rat cardiac trabeculae. [Ca2+]i was measured using electrophoretically injected fura 2 and an image-intensified charge-coupled device camera. PGJ was calculated from the diffusion coefficient for fura 2 in trabeculae (Dtrab) and in the myoplasm (Dmyop). After 1- and 3-h superfusion with 100 µM 1-octanol, Dmyop showed no significant changes, whereas Dtrab was reduced significantly. Therefore, calculated PGJ was reduced from 4.15 × 10-5 to 2.10 × 10-5 and 0.86 × 10-5 cm/s, respectively. The propagation velocity of the regional increases in [Ca2+]i during TPCs was constant, averaging 1.69 ± 1.48 mm/s (range 0.34-5.47 mm/s, n = 10). These observations support the hypothesis that TPCs are initiated near the damaged ends of trabeculae and are propagated by CICR from the sarcoplasmic reticulum mediated by diffusion of Ca2+ through cells and from cell to cell through GJs.

rat cardiac trabeculae; octanol


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