| Abstract
| - We have recently described that local contractions can be triggered by a preceding twitch in rat cardiac trabeculae in or near damaged ends of the muscle. These local contractions appeared to propagate along the trabeculae with a constant velocity; hence, they can be denoted as triggered propagated contractions (TPCs). These studies have also shown that stretch and/or subsequent shortening of the damaged ends during the twitch is necessary for the induction of TPCs. Objectives: We tested in this study: (1) whether activation of stretch-activated channels in the damaged regions is involved in the initiation of TPCs; (2) whether activation of stretch-activated channels due to stretch of tissue adjacent to a local triggered contraction increases the velocity of propagation. As gadolinium (Gd3+) has been shown to be the most effective blocker of stretch-activated channels to date, we have studied the effects of Gd3+ on twitch force, as well as on force, triggering rate and propagation velocity of TPCs. Methods: TPCs were elicited by trains of 15 stimuli (2 Hz, 15-s intervals) at 20 °C; using HEPES solution, [Ca2+]0 of 0.5 ~ 0.75 mmol/l. Laser diffraction techniques were used to measure sarcomere shortening at two sites in the trabeculae; twitch force was measured with a silicon strain gauge. Results: Gd3+ (1 ~ 20 μmol/l) decreased both twitch force and force, triggering rate and propagation velocity of TPCs in a concentration-dependent manner. High concentrations of Gd3+ (>20 μmol/l) almost abolished both twitch force and triggered force. The decrease of triggering rate and velocity, for the same decrease in twitch force, were not significantly larger than those by decreasing [Ca2+]0, indicating that Gd3+ did not cause an additional effect on TPCs above decreasing intracellular [Ca2+]. Conclusion: These observations suggest that it is not necessary to assume that Gd3+ sensitive stretch-activated channels are involved in triggering or propagation of these local contractions.
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