The effect of oxyphenamone (Oxy, a new inodilator) on high energy phosphate metabolism of isolated Langendorff perfused rat hearts exposed to 60 minutes of ischemia and 60 minutes of reperfusion injury was determined using phosphorus nuclear magnetic resonance (³¹P NMR) spectroscopy. The results led to a paradox of rapid intracellular pH recovery and a low level of high energy phosphate pools reserve during reperfusion compared to the control. It can be stated that Oxy improves energy consumption and, in turn, improves pH recovery, but also causes a deletion of high energy phosphate pools during reperfusion. The relationship between ions regulation, including H^＋ regulation, and myocardial functions recovery may display a key factor for cell survival during postischemic reperfusion.