title: Recruitment of a time-dependent inotropic reserve by postextrasystolic potentiation in normal and reperfused myocardium.
abstract: Impaired excitation-contraction coupling has been suggested as the underlying mechanism of postischemic contractile dysfunction of reperfused myocardium in in-vitro studies. To test this hypothesis in situ, postextrasystolic potentiation (PESP) following an extrasystole with constant prematurity and three different postextrasystolic time intervals (compensated, regular, abbreviated) was analyzed in 12 anesthetized dogs. Changes in regional inotropic state were assessed by comparison of end-systolic wall thickness (sonomicrometry) during PESP to the respective pressure-matched values of an end-systolic pressure/wall-thickness relationship established during brief manual clamping of the aorta. Before ischemia, posterior end-systolic wall-thickness was increased by 0.19 +/- 0.35 (SD) mm during PESP with an abbreviated, by 0.36 +/- 0.42 mm with a regular, and by 0.60 +/- 0.42 mm with a compensated postextrasystolic interval. Baseline systolic wall thickening was decreased from 16.2 +/- 5.4% (before ischemia) to -3.0 +/- 3.4% at the end of 15 min left circumflex coronary occlusion, and to 2.8 +/- 7.5% at 10 min, 7.2 +/- 3.9% at 4 h, and 7.9 +/- 4.1% at 8 h reperfusion. Stepwise increases in regional inotropic state during PESP with increasing postextrasystolic intervals were not different in normal and reperfused myocardium. Thus, excitation-contraction coupling appears not to be impaired during inotropic stimulation of reperfused myocardium in situ.
authors.affiliation: Abteilung für Pathophysiologie, Universitätsklinikum Essen, FRG.
authors.forename: S
authors.initials: S
authors.lastname: Schäfer
authors.forename: G
authors.initials: G
authors.lastname: Heusch
mesh_terms: D000818:Animals; D004285:Dogs; D005260:Female; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D013599:Systole / Q000502:physiology