title: Pacing redistributes glycogen within the developing myocardium.
abstract: Electrical pacing at physiological rate induces myocardial remodeling associated with regional changes in workload, blood flow and oxygen consumption. However, to what extent energy-producing pathways are also modified within the paced heart remains to be investigated. Pacing could particularly affect glycogen metabolism since hypertrophy stimulates glycolysis and increased workload favors glucose over fat oxidation. In order to test this hypothesis, we used the embryonic chick heart model in which ventricular pacing rapidly resulted in thinning of the ventricle wall and thickening of the atrial wall. Hearts of stage 22HH chick embryos were submitted in ovo to asynchronous and intermittent ventricular pacing delivered at physiological rate during 24 h. The resulting alterations of glycogen content were determined in atrium, ventricle and conotruncus of paced and sham-operated hearts. Hemodynamic parameters of the paced and spontaneously beating hearts were derived from computerized image analysis of video recordings. With respect to sham, paced hearts showed a significant decrease in glycogen content (nmoles glucose units/microg protein; mean+/-S.D.) only in atrium (1.48+/-0.40 v 0.84+/-0.34, n=8) and conotruncus (0.75+/-0.28 v 0.42+/-0.23, n=8). Pacing decreased the end diastolic and stroke volumes by 34 and 44%, respectively. Thus, the rapid glycogen depletion in regions remote from the stimulation site appears to be associated with regional changes in workload and remodeling. These findings underscore the importance of the coupling mechanisms between metabolic pathways and myocardial remodeling in the ectopically paced heart.
authors.affiliation: Division of Cardiology, University Hospital, BH 16.309, 1011 Lausanne-CHUV, Switzerland. xlyon@hola.hospvd.ch
authors.forename: X
authors.initials: X
authors.lastname: Lyon
authors.forename: L
authors.initials: L
authors.lastname: Kappenberger
authors.forename: D
authors.initials: D
authors.lastname: Sedmera
authors.forename: A C
authors.initials: AC
authors.lastname: Rochat
authors.forename: P
authors.initials: P
authors.lastname: Kucera
authors.forename: E
authors.initials: E
authors.lastname: Raddatz
mesh_terms: D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D002642:Chick Embryo; D004558:Electric Stimulation; D006003:Glycogen / Q000378:metabolism*; D006321:Heart / Q000196:embryology* / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000378:metabolism*; D006439:Hemodynamics; D009206:Myocardium / Q000378:metabolism; D010138:Pacemaker, Artificial
chemical_list: D006003:Glycogen