Roles of intracellular Ca^<2+> in genesis of life-threatening arrhythmia.

豚鼠和Psts心室肌细胞分离的细胞质钙阶梯酶。采用Ca^<2+>敏感荧光染料fura2研究了单个心肌细胞胞浆钙浓度（[Ca^<2+>]）的动态变化，以阐明哺乳动物心脏张力阶梯现象的机制。在休息3分钟后，1.0 H_z的刺激训练在豚鼠肌细胞中产生(Ca^<2+>]i的上升阶梯，而在大鼠肌细胞中产生[Ca^<2+>]i的下降阶梯。在相同的刺激方案中，肌浆网（SR）抑制剂ryanodine （1 μ m）显著降低了大鼠肌细胞中[Ca^<2+>]i的水平，而对豚鼠肌细胞中[Ca^<2+>]i的瞬态没有明显影响。这些结果表明，在大鼠肌细胞中，SR在负性收缩阶梯现象的发生中起重要作用，而在豚鼠肌细胞中，Ca^<2+>在肌膜上的运动在正性收缩阶梯现象的发生中更重要。单豚鼠肌细胞氧化磷酸化恢复后胞质钙浓度（[Ca^<2+>]i）的波动。使用Ca^<2+>敏感荧光染料fura2，在单豚鼠肌细胞中检测氧化磷酸化恢复后[Ca^<2+>]i瞬态的动力学，以阐明再灌注心律失常的机制。暴露于DNP(0.1 mM) 5分钟后，氧化磷酸化的恢复引起收缩和舒张[Ca^<2+>]i的显著升高，并伴有[Ca^<2+>]i在空间和几何上的不均匀波动，同时伴有自发收缩波和膜电位的波动。在冲洗溶液中加入ryanodine(1uM)，几乎完全消除了[Ca^<2+>]i和膜电位波动的发生。这些结果表明，肌浆网Ca^<2+>释放参与了氧化磷酸化恢复后发生的[Ca^<2+>]i和膜电位的波动。少

Cytosolic Calcium Stairacase in Ventricular Myocytes Isolated from Guinea-pigs and Psts. Dynamic changes in cytosolic calcium concenyration ([Ca^<2+>]) in single myocytes were investigated using a ca^<2+> sensitive fluorescence dye, fura2, to elucidate the mechanism of the tension staircase phenomenon of mammalian hearts. A stimulation train at 1.0 H_z after a 3 min rest period produced an ascending staircase of (Ca^<2+>]i transients in guinea-pig myocytes, while a descending staircase of [Ca^<2+>]i transients in rat myocytes. During the same stimulation protocol, an inhibitor of the sarcoplasmic reticulum (the SR), ryanodine (1 uM), sigh, ficantly depressed the leve of [Ca^<2+>]i in rat myocytes, while did not appreciably affected [Ca^<2+>]i transients in guinea-pig myocytes. These results suggested that in rat myocytes the SR plays important role in the genesis of the negative contractile staircase phenomenon, while in guinea-pig myocytes the Ca^<2+> movement across the salcolemma is … More important for the genesis of the positive contractile staircase phenomenon.Flutuation of Cytosolic Calcium Concentration ([Ca^<2+>]i) Following Resumption of Oxidative phosphorylation in Single Guinea-pig Myocytes.Dynamics of [Ca^<2+>]i transients following resumption of oxidative phosphorylation were examined in single guinea-pig myocytes using a Ca^<2+>-sensitive fluorescent dye, fura2, in order to elucidate mechanisms of the reperfusion arrhythmia. Resumption of oxidative phosphorylation, produced by a wash-out after 5-min exposure to DNP(0.1 mM), caused a significant rise of both systolic and diastolic [Ca^<2+>]i associated with spatially and gemetrically inhomogenous fluctuations of [Ca^<2+>]i, which were accompanied by the spontaneous contractile wave and fluctuation of the membrane potential. An addition of ryanodine(1uM) to the wash-out solution, almost completely abolished the occurrence of both the [Ca^<2+>]i and membrane potential fluctuations. These results suggest that the Ca^<2+> release from the sarcoplasmic reticulum is involved in the fluctuation of [Ca^<2+>]i and membrane potential that occurs following resumption of oxdative phosphorylation. Less