title: Ca(2+)-free, high-Ca2+ coronary perfusion suppresses contractility and excitation-contraction coupling energy.
abstract: We studied the mechanoenergetic effects of a short-term Ca(2+)-free, high-Ca2+ Tyrode solution coronary perfusion in eight excised, cross-circulated canine hearts. The perfusion protocol consisted of coronary perfusion with Ca(2+)-free Tyrode solution for 10 min followed by high-Ca2+ (16 mM) Tyrode solution for 5 min. This new protocol successfully induced acute contractile failure in seven hearts, without myocardial ultrastructural changes. We studied the end-systolic pressure-volume relation (slope = Emax, a contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA) in these failing hearts. These hearts had no increase in end-diastolic pressure at a given volume, a 40% decrease in Emax and a proportional decrease in the PVA-independent VO2 for 1-4 h, but no decrease in the oxygen cost of PVA, defined as the slope of the VO2-PVA relation. The oxygen cost of Emax for Ca2+ handling, defined as the slope of the relation between PVA-independent VO2 and Emax, was unchanged in the failing hearts. We conclude that the present protocol induced left ventricular contractile failure, primarily involving the suppression of Ca2+ handling energy for excitation-contraction coupling.
authors.affiliation: Second Department of Physiology, Okayama University Medical School, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Araki
authors.forename: M
authors.initials: M
authors.lastname: Takaki
authors.forename: T
authors.initials: T
authors.lastname: Namba
authors.forename: M
authors.initials: M
authors.lastname: Mori
authors.forename: H
authors.initials: H
authors.lastname: Suga
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D002118:Calcium / Q000008:administration & dosage / Q000494:pharmacology*; D003427:Cross Circulation; D004195:Disease Models, Animal; D004285:Dogs; D004734:Energy Metabolism / Q000187:drug effects; D006321:Heart / Q000187:drug effects / Q000502:physiology; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology; D066298:In Vitro Techniques; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure; D010101:Oxygen Consumption; D010477:Perfusion; D012996:Solutions
chemical_list: D012996:Solutions; D002118:Calcium