Impaired tolerance to ischemia-reperfusion in older hearts may stem in part from alterations
in purine catabolism, impacting on maintenance of energy state and protective signaling via
extracellular adenosine. We characterized effects of aging on normoxic and post-ischemic
purine metabolism in hearts from young (2–4 month), middle-aged (12 month), old (18
month), and senescent (24–28 month) C57/Bl6 mice. Normoxic function was similar in all
age groups while normoxic purine efflux increased gradually with age. This was the result of …