CA2+ WAVES DURING TRIGGERED PROPAGATED CONTRACTIONS IN INTACT TRABECULAE

Triggered propagated contractions (TPCs) starting from damaged regions travel along multicellular cardiac muscle preparations. We have repor ted that octanol (100 mu M) inhibits TPCs. The inhibitory effect of oc tanol on propagation of TPCs could be due to an effect of octanol on C a2+-induced Ca2+ release (CICR) mediated by Ca2+ diffusion inside the single cell or on the diffusion of Ca2+ from cell to cell via gap junc tions (GJs). Therefore, we studied the regional changes in intracellul ar Ca2+ concentration ([Ca2(+)](i)) during TPCs and the effect of octa nol on the permeability of gap junctions (P-GJ) in rat cardiac trabecu lae. [Ca2+](i) was measured using electrophoretically injected fura 2 and an image-intensified charge-coupled device camera. P-GJ was calcul ated from the diffusion coefficient for fura 2 in trabeculae (D-trab) and in the myoplasm (D-myop). After 1- and 3-h superfusion with 100 mu M 1-octanol, D-myop showed no significant changes, whereas D-trab was reduced significantly. Therefore, calculated P-GJ was reduced from 4. 15 x 10(-5) to 2.10 x 10(-5) and 0.86 x 10(-5) cm/s, respectively. The propagation velocity of the regional increases in [Ca2+](i) during TP Cs 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 initia ted near the damaged ends of trabeculae and are propagated by CICR fro m the sarcoplasmic reticulum mediated by diffusion of Ca2+ through cel ls and from cell to cell through GJs.