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-microL 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 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 approximately 2 min). Action potential shortened in duration at 50% repolarization by approximately 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 (approximately 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 beta-stimulated (1 microM 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 (approximately 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 suggests an increased Ca2+ recirculation through the sarcoplasmic reticulum between two consecutive beats (35% before Triton vs. 45% after Triton).(ABSTRACT TRUNCATED AT 250 WORDS)
Bourreau
J P
JP
Department of Physics, The University of Calgary, AB, Canada.
Banijamali
H S
HS
Challice
C E
CE
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D009202:Cardiomyopathies / Q000503:physiopathology*; D002415:Cats; D004699:Endocardium / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D006331:Heart Diseases / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D009206:Myocardium / Q000166:cytology; D017830:Octoxynol / Q000494:pharmacology; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D012433:Ryanodine / Q000494:pharmacology; D013599:Systole / Q000502:physiology; D013997:Time Factors; D016276:Ventricular Function
D012433:Ryanodine; D017830:Octoxynol; D011188:Potassium