title: The phosphocreatine overshoot occurs independent of myocardial work.
abstract: Although the exact mechanism(s) responsible for the phosphocreatine/ATP overshoot have not been completely elucidated, our data demonstrate that the overshoot does not stem from reduced myocardial work, and consequently, reduced utilization of phosphocreatine (PCr). Additionally, we highlight a basic difference in the physiologic responses of skeletal and cardial muscle to work demands. By understanding the bioenergetic derangements which accompany reperfusion injury, one may hope to better salvage post-ischemic myocardium.
authors.affiliation: Medical College Hospital, Department of Surgery, Philadelphia, PA 19129, USA.
authors.forename: L J
authors.initials: LJ
authors.lastname: Kaplan
authors.forename: C F
authors.initials: CF
authors.lastname: Bellows
authors.forename: S
authors.initials: S
authors.lastname: Carter
authors.forename: H
authors.initials: H
authors.lastname: Blum
authors.forename: G J
authors.initials: GJ
authors.lastname: Whitman
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis / Q000502:physiology*; D000818:Animals; D004734:Energy Metabolism; D006321:Heart / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000737:chemistry / Q000502:physiology*; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010725:Phosphocreatine; D000255:Adenosine Triphosphate