title: Frank-Starling mechanism retains recirculation fraction of myocardial Ca(2+) in the beating heart.
abstract: Myocardial Ca(2+) handling in excitation-contraction coupling is the second primary determinant of energy or O(2) demand in a working heart. The intracellular and extracellular routes remove myocardial Ca(2+) that was released into the sarcoplasma with different Ca(2+): ATP stoichiometries. The intracellular route is twice as economical as the extracellular route. Therefore the fraction of total Ca(2+) removed via the sarcoplasmic reticulum, i.e., the recirculation fraction of intracellular Ca(2+) (RF), determines the economy of myocardial Ca(2+) handling. RF has conventionally been estimated as the exponential decay rate of postextrasystolic potentiation (PESP). However, we have found that PESP usually decays in alternans, but not exponentially in the canine left ventricle beating above 100 beats/min. We have succeeded in estimating RF from the exponential decay component of an alternans PESP. We previously found that the Frank-Starling mechanism or varied ventricular preload did not affect the economy of myocardial Ca(2+) handling. Then, to account for this important finding, we hypothesized that the Frank-Starling mechanism would not affect RF at a constant heart rate. We tested this hypothesis and found its supportive evidence in 11 canine left ventricles. We conclude that RF at a constant heart rate would remain constant, independent of the Frank-Starling mechanism.
authors.affiliation: Department Cardiovascular Physiology II, Okayama University Graduate School of Medicine and Dentistry, Okayama, 700-8558 Japan.
authors.forename: J
authors.initials: J
authors.lastname: Mizuno
authors.forename: J
authors.initials: J
authors.lastname: Araki
authors.forename: S
authors.initials: S
authors.lastname: Mohri
authors.forename: H
authors.initials: H
authors.lastname: Minami
authors.forename: Y
authors.initials: Y
authors.lastname: Doi
authors.forename: W
authors.initials: W
authors.lastname: Fujinaka
authors.forename: K
authors.initials: K
authors.lastname: Miyaji
authors.forename: T
authors.initials: T
authors.lastname: Kiyooka
authors.forename: Y
authors.initials: Y
authors.lastname: Oshima
authors.forename: G
authors.initials: G
authors.lastname: Iribe
authors.forename: M
authors.initials: M
authors.lastname: Hirakawa
authors.forename: H
authors.initials: H
authors.lastname: Suga
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004285:Dogs; D004734:Energy Metabolism / Q000502:physiology; D006321:Heart / Q000502:physiology*; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D016276:Ventricular Function; D018879:Ventricular Premature Complexes / Q000503:physiopathology; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D000255:Adenosine Triphosphate; D002118:Calcium