Metabolic protection of post-ischemic phosphorylation potential and ventricular performance.
Relationships between cytosolic phosphorylation potential, low-flow ischemic purine release and post-ischemic left ventricular developed pressure were examined in perfused working guinea-pig heart. During moderate ischemic acidification, metabolic intervention by pyruvate attenuated cytosolic NADH accumulation and (ATP+ADP+AMP) degradation. In reperfusion, spontaneously developed ventricular pressure increased in parallel with the phosphorylation potential (R2 = 0.71), but forced restoration of function by inotropic measures occurred at the expense of the phosphorylation potential.
Mallet
R T
RT
Department of Physiology, Texas College of Osteopathic Medicine, Fort Worth 76107-2699.
Bünger
R
R
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D003326:Coronary Circulation / Q000502:physiology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D009243:NAD / Q000378:metabolism; D010766:Phosphorylation; D011773:Pyruvates / Q000494:pharmacology; D019289:Pyruvic Acid; D016277:Ventricular Function, Left / Q000502:physiology*
D002316:Cardiotonic Agents; D011773:Pyruvates; D009243:NAD; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate