title: Total Ca handling in canine mild Ca overload failing heart.
abstract: We analyzed total Ca handling of the left ventricle (LV) in the mildly failing heart preparation induced by a temporary intracoronary Ca overloading intervention in eight excised and cross-circulated canine hearts. This Ca intervention consisted of interruption of coronary blood perfusion by Ca-free oxygenated Tyrode perfusion for 10 min followed by high-Ca (16mmol/l) oxygenated Tyrode perfusion for 5 min. This intervention decreased the LV contractility index, Emax (end-systolic maximum elastance), by 40% after restoration of the blood cross-circulation. We expected a Ca overload or paradox failing heart resembling the postischemic stunned heart and being characterized by an increased O2 cost of Emax. However, LV O2 consumption under mechanically unloading conditions decreased by 30% from control without increasing the O2 cost of Emax. To obtain a mechanistic view of this failing heart, we investigated cardiac total Ca handling by our integrative analysis method. In this method, we obtained the internal Ca recirculation fraction (RF) from the decay beat constant of the postextrasystolic potentiation following each sporadic spontaneous extrasystole in these failing LVs. We combined the RF with the decreased Emax and the unchanged O2 cost of Emax in our recently developed formula of total Ca handling. We found that these failing LVs had a slightly but significantly increased RF accompanied by either a slightly increased futile Ca cycling or a slightly decreased Ca reactivity of Emax, or both. Any of these three possible changes can account for the unchanged O2 cost of Emax. This result indicates that the present mildly failing heart has not yet fallen into a typical Ca overload or paradox by the temporary Ca overloading intervention.
authors.affiliation: Department of Physiology II, Okayama University Medical School, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Mizuno
authors.forename: J
authors.initials: J
authors.lastname: Araki
authors.forename: G
authors.initials: G
authors.lastname: Iribe
authors.forename: M
authors.initials: M
authors.lastname: Maesako
authors.forename: T
authors.initials: T
authors.lastname: Morita
authors.forename: K
authors.initials: K
authors.lastname: Miyaji
authors.forename: T
authors.initials: T
authors.lastname: Imaoka
authors.forename: S
authors.initials: S
authors.lastname: Mohri
authors.forename: S
authors.initials: S
authors.lastname: Sano
authors.forename: T
authors.initials: T
authors.lastname: Ohe
authors.forename: M
authors.initials: M
authors.lastname: Hirakawa
authors.forename: H
authors.initials: H
authors.lastname: Suga
mesh_terms: D000818:Animals; D001665:Binding Sites; D001784:Blood Gas Analysis; D002118:Calcium / Q000378:metabolism* / Q000633:toxicity; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D006333:Heart Failure / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D066298:In Vitro Techniques; D007552:Isotonic Solutions / Q000633:toxicity; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion / Q000379:methods
chemical_list: D007552:Isotonic Solutions; C037692:Tyrode's solution; D002118:Calcium