The phosphocreatine overshoot occurs independent of myocardial work.
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.
Kaplan
L J
LJ
Medical College Hospital, Department of Surgery, Philadelphia, PA 19129, USA.
Bellows
C F
CF
Carter
S
S
Blum
H
H
Whitman
G J
GJ
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
D010725:Phosphocreatine; D000255:Adenosine Triphosphate