Myocardial energy restoration of ischemic damage by administration of phosphoenolpyruvate during reperfusion. A study in a paracorporeal rat heart model.
The myocardial energy restoration of ischemic damage by administration of phosphoenolpyruvate during reperfusion was investigated in a paracorporeal heart model modified in the rat. Excised hearts were subjected to 15 min of complete global ischemia at ischemia at 37 degrees C before pulsatile blood reperfusion for 30 min. One group (n = 7) was supplemented with 67 mumol of phosphoenolpyruvate and 0.67 mumol of adenosine triphosphate dissolved in 10 ml of saline and another with plain saline (nonsupplemented) during reperfusion. All hearts were freeze-clamped after 30 min of reperfusion and subjected to energy content analysis. The adenylate charge potential was 0.91 +/- 0.01 (mean +/- SD) for the supplemented and 0.85 +/- 0.06 (mean +/- SD) for the nonsupplemented group. This difference was significant (p less than 0.02). Concomitantly the outflow of creatine kinase was less for the supplemented group. The translocation of phosphoenolpyruvate into the myocardial cells seems possible by blood supplementation of a lower dose of adenosine triphosphate.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism; D004734:Energy Metabolism; D006321:Heart / Q000187:drug effects*; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010728:Phosphoenolpyruvate / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D010728:Phosphoenolpyruvate; D000255:Adenosine Triphosphate; D003402:Creatine Kinase