EFFECTS OF NITRIC OXIDE ON MYOCRADIAL CONTRACTION-CALCIUM DEPENDENT MECHANISM AND ITS SIGNIFICANTROLEIN ISCHEMIC REPERFUSION MYOCARDIAL DAMAGE

（一）.本研究的主要目的是确定内源性一氧化氮（NO）的抑制是否会增强可逆性缺血后心肌功能障碍，即心肌顿抑。冠状动脉内注射N-硝基-L-精氨酸（L-NA）不影响全身血流动力学，透壁心肌血流量仅在输注区域略有减少，但有显著性。与无L-NA组相比，L-NA组内、外膜下心肌顿抑均增强，且心肌顿抑的增强与心肌血流量的减少不成比例。因此，通过抑制NO增强心肌顿抑的机制似乎与其对血流的影响无关。（二）、本研究的第二个目的是确定抑制NO是否通过Ca^2+依赖性机制增强期外收缩后增强（PESP），PESP是兴奋-收缩偶联的生理指标之一。L-NA不影响基础LV dP/dt，也不增加PESP，Ryanodine以剂量依赖的方式降低PESP，额外的CaCl 2部分恢复PESP。在Ryanodine存在下，L-NA增强CaCl 2对基础LV dP/dt的影响，但不增强PESP。在ryanodine存在的情况下，NO合成的抑制增强了外部Ca^2+的变力作用，但不增强PESP，PESP主要依赖于肌浆网释放的细胞内Ca^2+。

(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.