Modification of excitation–contraction coupling in cat ventricular myocardium following endocardial damage

Damage to endocardial endothelium (denudation of the superficial tissue) by brief exposure to a 100-μL bolus of detergent (Triton X-100, 1% by volume stock) decreased the twitch force of papillary muscle (and trabeculae) by ~ 30% to a new but steady level without changes in resting tension. The decline in twitch force was evident immediately after the addition of Triton. Modification of the action potential measured from the contracting tissue appeared only later, when the change in contraction was already well established (i.e., after ~ 2 min). Action potential shortened in duration at 50% repolarization by ~ 100 ms and increased in plateau amplitude, although the latter increase was not always observed. A similar treatment procedure applied to strips of ventricular wall with the endocardium exposed to the superfusion solution resulted in a substantial decrease in action potential duration (~ 110 ms). In contrast, treatment of strips of epicardial layers of ventricular walls (with epicardial side facing the superfusion solution) did not produce a similar result. In β-stimulated (1 μM isoproterenol) and partially depolarized preparations (with 20 mM KCl), with intact endocardium, electrically evoked contractions were followed by aftercontractions, which were suppressed following Triton treatment. Action potentials in a depolarizing medium also shortened in duration (~ 50 ms), although following a delay (2–3 min). The decay to steady state of postextrasystolic potentiated beat was slower after endocardial damage than under control conditions. This suggested an increased Ca2+ recirculation through the sarcoplasmic reticulum between two consecutive beats (35% before Triton vs. 45% after Triton). Finally, in a medium containing 3 μM ryanodine, Triton treatment of the endocardial endothelium failed to induce any effect on either twitch force or action potential. Prolonged exposure to Triton X-100 (by a slow flow or high concentration) induced only deteriorating effects leading to substantial rise in the resting tension and generation of contractures and abbreviated action potentials with depressed plateau. These observations are consistent with the hypothesis that a modification in the sarcoplasmic reticulum function may, at least in part, be responsible for the observed changes in contractile function of the myocardium following endocardial damage with Triton treatment.Key words: endocardial endothelium, sarcoplasmic reticulum, ventricle, myocardial contraction.