Baboon hearts were preserved ex vivo after hypothermic ischemic or cardioplegic arrest and were stored cold (0.5 degrees C) for 24 hours. Ischemic arrest was induced on cardiopulmonary bypass after general cooling to 25 degrees C. Cardioplegic arrest was induced using either a hyperkalemic standard cardioplegic solution National Institutes of Health [( NIH] solution) or the recently developed University of Wisconsin (UW) organ preservation solution. ATP and catabolites were assessed in serial transmural biopsies. Cardioplegia significantly delayed the breakdown of ATP during storage. After infusion of the adenosine-supplemented UW solution, myocardial content of adenosine was high as compared with that in NIH-arrested hearts (9.12 versus 0.01 mumol.g-1 dry wt). During cold storage, however, adenosine converted to inosine in spite of profound hypothermia. This renders unlikely the potential of fast resynthesis of ATP out of the supplemented nucleoside pool after reoxygenation.