Purine and pyrimidine catabolite production in the postischemic rat heart--effect of adenosine supply during reperfusion.

Abstract

Marked reduction in purine catabolite production is invariably observed in the course of repeated ischemic events1–3. Both beneficial and deleterious effects of this phenomenon should be taken into consideration. Inhibition of nucleotide breakdown protects the nucleotide pool particularly ATP in the heart but at the expense of the reduction of the release of endogenous protective metabolite — adenosine (ADO). Exogenous ADO exerts a significant reviving effect on the heart when supplied during reperfusion4–6 which may be partially mediated by substitution for impaired release of endogenous ADO. Exogenous ADO is also the most efficiently used substrate for resynthesis of adenine nucleotides. To obtain further information concerning the mechanism producing beneficial effect of ADO supplied during reperfusion we investigated the effects of three concentrations of ADO (optimal for vasoactive, metabolic and cardioplegic effect) on mechanical recovery, myocardial nucleotides and purine and pyrimidine catabolite production in Langendorff perfused rat heart.KeywordsMyocardial StunningNucleotide PoolDevelop TensionMyocardial Reperfusion InjuryImpaired ReleaseThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.