MODIFICATION OF EXCITATION-CONTRACTION COUPLING IN CAT VENTRICULAR MYOCARDIUM FOLLOWING ENDOCARDIAL DAMAGE

Damage to endocardial endothelium (denudation of the superficial tissu e) by brief exposure to a 100-muL bolus of detergent (Triton X-100, 1% by volume stock) decreased the twitch force of papillary muscle (and trabeculae) by approximately 30% to a new but steady level without cha nges in resting tension. The decline in twitch force was evident immed iately after the addition of Triton. Modification of the action potent ial measured from the contracting tissue appeared only later, when the change in contraction was already well established (i.e., after appro ximately 2 min). Action potential shortened in duration at 50% repolar ization by approximately 100 ms and increased in plateau amplitude, al though the latter increase was not always observed. A similar treatmen t procedure applied to strips of ventricular wall with the endocardium exposed to the superfusion solution resulted in a substantial decreas e in action potential duration (approximately 110 ms). In contrast, tr eatment of strips of epicardial layers of ventricular walls (with epic ardial side facing the superfusion solution) did not produce a similar result. In beta-stimulated (1 muM isoproterenol) and partially depola rized preparations (with 20 mM KCl), with intact endocardium, electric ally evoked contractions were followed by aftercontractions, which wer e suppressed following Triton treatment. Action potentials in a depola rizing medium also shortened in duration (approximately 50 ms), althou gh following a delay (2 - 3 min). The decay to steady state of postext rasystolic potentiated beat was slower after endocardial damage than u nder control conditions. This suggested an increased Ca2+ recirculatio n through the sarcoplasmic reticulum between two consecutive beats (35 % before Triton vs. 45% after Triton). Finally, in a medium containing 3 muM ryanodine, Triton treatment of the endocardial endothelium fail ed to induce any effect on either twitch force or action potential. Pr olonged exposure to Triton X-100 (by a slow flow or high concentration ) induced only deteriorating effects leading to substantial rise in th e resting tension and generation of contractures and abbreviated actio n 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 chang es in contractile function of the myocardium following endocardial dam age with Triton treatment.