Basal metabolism does not account for high O2 consumption in stunned myocardium.

Myocardial O2 consumption (MV˙o 2) in stunned myocardium is relatively high compared with the reduced ventricular function. The mechanism of this "oxygen paradox" could occur at different levels: basal metabolism, excitation-contraction coupling, and energy production. In one previously reported series on 12 isolated, blood-perfused rabbit hearts, left ventricular systolic and diastolic function in stunned myocardium were significantly decreased compared with control, whereas total MV˙o 2 was not. The MV˙o 2 for the unloaded contraction was overproportionately high for the decreased function in stunned myocardium, and contractile efficiency was clearly deteriorated. To assess whether the basal metabolism specifically is elevated in stunned myocardium, a second series ( n =14) with a similar protocol was performed in this study. Basal MV˙o 2 after KCl arrest (0.5 ± 0.3 ml ⋅ min-1 ⋅ 100 g-1) was significantly lower than that measured after KCl arrest (1.2 ± 0.5 ml ⋅ min-1 ⋅ 100 g-1) in an additional series on nonischemic hearts ( n = 8). Our conclusion is that basal MV˙o 2 in stunned myocardium is not elevated. Thus this O2-consuming portion of total MV˙o 2 is not responsible for the inefficiency in stunned myocardium. Instead, a "metabolic stunning" occurs at the level of both excitation-contraction coupling and force development by the contractile apparatus.