| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
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| Research Abstract |
(1). The primary goal of the present investigation was to determine whetherinhibition of endogenous nitric oxide (NO) enhances reversible postischemicmyocardial dysfunction, ie, myocardial stunning. Intracoronary administration of N-nitro-L-arginine (L-NA) did not affect systemic hemodynamics, and transmural myocardial blood flow was reduced slightly but significantly only in the infusion territory. Myocardial stunning was enhanced not only in the subendocardium but also in the subepicardiumin in the presence of L-NA compared with the absence of L-NA.The enhancement of myocardial stunning was out of proportion with the reduction of myocardial blood flow. Thus, the mechanism of enhancement of myocardial stunning by inhibition of NO seemed to be potentially independent of its effects on blood flow.
(2). The second goal of the present study was to determine whether inhibition of NO enhances post-extrasystolic potentiation (PESP), one of the physiological indices of excitation-contraction coupling, through a Ca^<2+>dependent **echanisum. L-NA neither affected baseline LV dP/dt nor enhanced PESP.Ryanodine diminished PESP in a dose dependent fashion, and an additional CaCl2 partially restoredit. In the presence of ryanodine, the effect of CaCl2 on baseline LV dP/dt was enhanced by L-NA,however, PESP was not enhanced. Inhibition of NO synthesis enhances the inotropic effect of extemal Ca^<2+> in the presence of ryanodine, but does not enhance PESP,which depends mainly upon intracellular Ca^<2+> release from sarcoplasmicreticulm.
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