Abstract

Solutions of adenosine triphosphate (ATP) were injected into the left coronary artery of isolated nonperfused dog hearts kept for 30 to 180 minutes at temperatures varying from 4 to 34°C. The amount of ATP administered varied from 0.5 to 7 µmoles/g heart. The left ventricles of the ATP-treated hearts had a higher content of adenine nucleotides and of phosphocreatine than did the left ventricles of control hearts not exposed to ATP. This effect was temperature-dependent and was maximal at 14°C. Glycogen disappearance in the hypothermic myocardial tissue was markedly slowed in a dose-dependent fashion by the administration of ATP. Injections of adenine and adenosine were without effect. An analysis of the intra- and extracellular distribution of simultaneously administered adenosine-8 -14 C-triphosphate and adenosine triphosphate-α- 32 P shows that the injected ATP was mainly split into ADP, AMP, adenosine, and inorganic phosphate and indicates that a minor percentage of these fission products entered the myocardial cells, some of the ADP and AMP being rephosphorylated there to ATP. The results suggest that intravascular introduction of ATP into the arrested hypothermic heart might help in the survival of the organ.

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