AbstractThe present study was performed to determine whether31P NMR relaxation times (T1) of adenosine triphosphate (ATP) might be used to monitor the resultant altered myocardial physiology produced by ischemia and possibly to explain mechanisms of altered physiology. To this end, pre‐and post‐ischemicT1s were determined in hearts perfused in the Lan‐gendorff mode, using31P NMR inversion recovery methods. In hearts without any pretreatment (CON), post‐ischemic ATP Ti values were significantly decreased compared with pre‐isch‐emic values (P<0.05): Pre‐isch: γ = 0.58 ± 0.08; α = 62 ± 0.06; β = 0.38 ± 0.08; Post‐isch: γ = 0.33 plusmn; 0.05; α = 0.43 ± 0. 03; β = 0. 23 plusmn; 0.05. In groups pretreated with creatine (CR), cyclocreatine (CY), or superoxide dismutase plus catalase (SOD‐CAT) before ischemia, the post‐ischemic ATPT1values were simlilar and were not significantly changed from pre‐ischemic values. These combined data suggest thatT1s of ATP might be used to monitor altered myocardial physiology and could provide insigh
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