Hemodynamic, electrocardiographic, and metabolic effects of fructose diphosphate on acute myocardial ischemia.
The hemodynamic, electrocardiographic, and metabolic responses of dogs with acute myocardial ischemia to intravenous administration of fructose-1,6-diphosphate (FDP) were assessed. Analysis of the results (compared to dextrose control) revealed evidence of major improvement of LVEDP and cardiac output, significant decrease of the ST segment, and large increases of ATP and CP in the ischemic district and to a lesser degree in the normally perfused myocardium. These results indicate that FDP intervenes in the Embden-Meyerhof pathway not only as a high energy substrate but also as a metabolic regulator influencing the activity of phosphofructokinase and that of pyruvate kinase. FDP also stimulates glycolysis in dog erythrocytes and increases their ATP and 2-3 DPG content by a factor of 2. The most significant finding in these studies is that this biochemical intervention appears to restore the depressed activity of glycolysis in ischemic myocardium.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism*; D004285:Dogs; D004562:Electrocardiography; D005635:Fructosediphosphates / Q000494:pharmacology*; D006439:Hemodynamics; D006598:Hexosediphosphates / Q000494:pharmacology*; D006651:Histocytochemistry; D007773:Lactates / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism
D005635:Fructosediphosphates; D006598:Hexosediphosphates; D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate