title: Effect of acetylsalicylic acid on metabolism and contractility in the ischemic reperfused heart.
abstract: The effect of acetylsalicylic acid (ASA) on high-energy phosphates (adenosine triphosphate: ATP, creatine phosphate: CrP, inorganic phosphate: Pi) and intracellular pH during myocardial ischemia and reperfusion was studied using phosphorus 31-nuclear magnetic resonance (31P-NMR) in the isolated rabbit hearts. Coronary flow, left ventricular systolic developed pressure (LV Dev.P) and left ventricular end-diastolic pressure (LVEDP) were also measured. Langendorff hearts perfused at 37 degrees C with the perfluorochemical emulsion Fluosol-43 were subjected to 15 min and 30 min of zero-flow ischemia and to 15 min of low-flow ischemia (coronary perfusion pressure = 20 mmHg) followed by 65 min of reperfusion (control, Group I). ASA (0.28 mmol/L) was infused either for the entire experimental period from beginning 45 min prior to ischemia (Group II) and infused immediately after reperfusion (Group III). During ischemia, Group II showed a significant suppression of the decrease in the ATP level and pH with both zero-flow and low-flow ischemia compared to those in the other groups, and moreover the increase in Pi and the decrease in CrP in low-flow ischemia were also suppressed. In Group III, the ATP level during reperfusion was significantly higher than that in Group I, but was not significantly different from that in 30 min zero-flow ischemia. In 30 min zero-flow ischemia, Pi, CrP and coronary flow after reperfusion in Group II tended to recover to preischemic values. There were no differences in LV Dev.P among the 3 groups. In conclusion, ASA has a protective effect on myocardial high-energy phosphates during ischemia and reperfusion in rabbit hearts.
authors.affiliation: First Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kawabata
authors.forename: K
authors.initials: K
authors.lastname: Sugiyama
authors.forename: R
authors.initials: R
authors.lastname: Katori
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D002097:C-Reactive Protein / Q000378:metabolism; D003331:Coronary Vessels / Q000502:physiology; D004734:Energy Metabolism / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D009119:Muscle Contraction / Q000187:drug effects*; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism; D010477:Perfusion; D010710:Phosphates / Q000378:metabolism; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D011817:Rabbits; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D010710:Phosphates; D010975:Platelet Aggregation Inhibitors; D015121:6-Ketoprostaglandin F1 alpha; D000255:Adenosine Triphosphate; D002097:C-Reactive Protein; D001241:Aspirin