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We investigated the effect of a novel cardioprotective agent, JTV-519, with or without a nitric oxide synthase inhibitor, L-NAME, on the myocardial metabolism and contraction during ischemia and reperfusion by means of phosphorus 31-nuclear magnetic resonance ( lated compounds during the ischemic period, could be blamed. Nonetheless, even in cases in which ATP does not decrease and creatine phosphate recovers rapidly after short periods of ischemia, stunning is already present. The fact that the stunned myocardium can respond well to inotropic stimulation by the dopamine, isoproterenol, calcium infusion, epinephrine, or postextrasystolic potentiation suggests that stunning represents a lack of available intracellular calcium, a failure of uptake of calcium by the sarcoplasmic reticulum, or a failure of the contractile proteins to respond to normal calcium concentration (2). Kusuoka et al. (3,4)

We investigated the effects of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, pravastatin, an angiotensin converting enzyme (ACE) inhibitor, temocaprilat, and an angiotensin II type 1 (AT1) receptor antagonist, CV-11974, on myocardial metabolism during ischemia in isolated rabbit hearts using phosphorus 31-nuclear magnetic resonance ( 31 P-NMR) imaging. Forty-five minutes of continuous normothermic global ischemia was carried out. Pravastatin, temocaprilat, CV-11974 or a nitric oxide synthase inhibitor, L-NAME was administered from 60 min prior to the global ischemia. Japanese white rabbits were divided into the following experimental groups, a control group (n 7), a group treated with pravastatin (P group; n 7), a group treated with pravastatin and temocaprilat (P T group; n 7), a group treated with pravastatin and CV-11974 (P CV group; n 7), and a group treated with pravastatin and L-NAME (P L-NAME group; n 7). During ischemia, P group, as well as either P T group or P CV group, showed a significant inhibition of the decreases in adenosine triphosphate (ATP) and intracellular pH (pHi) (p 0.01, respectively, at the end of ischemia compared to the control group as well as P L-NAME group), and a significant inhibition of the increase in inorganic phosphate (Pi) (p 0.01, respectively, compared with the control group as well as P L-NAME group). These results suggest that pravastatin significantly improved myocardial energy metabolism during myocardial ischemia. This beneficial effect was dependent on NO synthase.However, this beneficial effect was not enhanced by either temocaprilat or CV-11974.

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