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 (P(GJ)) in rat cardiac trabeculae. [Ca2+](i) was measured using electrophoretically injected fura 2 and an image- intensified charge-coupled device camera. P(GJ) was calculated 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 μM 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 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.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||1 43-1|
|Publication status||Published - 1998 Jan|
- Rat cardiac trabeculae
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)