PHASE RESETTING OF CIRCUS MOVEMENT REENTRY

马戏团运动再入通常作为一种机制被调用 室性心律失常，但起搏和持续的方式 重返大气层仍然是相当大的争论和猜测的主题。这个 这些研究的目的是确定再入和再入的决定因素 浦肯野-肌肉接头(PMJ)的作用机制 阈值以下电刺激、离子通道阻滞剂和自主神经 神经递质调节浦肯野肌肉再入。这些研究将 利用分枝浦肯野肌肉制剂安装在隔开的 巴斯。一个PMJ将与正常的Tyrode溶液进行超融合，另一个将与正常的Tyrode溶液进行超融合 PMJ将与高钾、低氧和酸性酪氨酸进行超融合 解决方案。将获得多个微电极记录 同时来自两个PMJ。再入大气层的预计组件 回路有：过早或过成熟的启动刺激；单向的 改变型TYRODE在PMJ处的顺行传导阻滞 解决方案；脉冲在功能障碍周围的循环 由于浦肯野和肌肉细胞之间缺乏电耦合，除了在 PMJ和；标记的逆行激活延迟和重返大气层 之前屏蔽了PMJ。这些活动的拟议机制是 PMJ的反射产生了一种过早的刺激，随后 启动再入，其中随着动作电位随时间的减少 幅度，由早期外向电流的恢复所调节，引起PMJ 传导阻断和随后的再入发展 成熟后的刺激。在尝试期间，PMJ处的传导阻滞 顺行传导是由较大的电气负荷引起的，或下沉到 肌肉产生的巨大来源。药物和神经递质 改变源和汇之间的关系可能会促进或抑制 相应地重新进入大气层。进一步的实验将检验这一假设 持续的浦肯野肌肉折返代表了一种生物振荡器，它 通过适当的时间安排，可以提前、延迟、拖累或消灭这一时期 传递给PMJ的亚阈值刺激。轨道的相平面轨迹 我们将对再入电路进行分析，以获得有关非线性的见解 重返大气层的行为。这些研究承诺通过以下方式来定义这些机制 它是启动和维持再入的，并提出了新的方法， 可以修改再入。

Circus movement reentry commonly has been invoke as a mechanism for ventricular arrhythmias, yet the modes of initiation and perpetuation of reentry remain the subject of considerable debate and conjecture. The purpose of these studies is to identify the determinants of reentry and Purkinje-muscle junctions (PMJ) and to establish the mechanisms by which subthreshold electrical stimuli,ionic channel blocking agents and autonomic neurotransmitters modulate Purkinje-muscle reentry. These studies will utilize branched Purkinje-muscle preparations mounted in a partitioned bath. One PMJ will be superfused with normal Tyrode solution and the other PMJ will be superfused with a hyperkalemic, hypoxic and acidotic Tyrode solution. Multiple microelectrode recordings will be obtained simultaneously from both PMJs. The projected components of the reentry circuit are: a premature or postmature initiating stimulus; unidirectional anterograde conduction block at the PMJ superfused with altered Tyrode solution; circulation of the impulse around the functional obstacle crated by lack of electrical coupling between Purkinje and muscle cells except at the PMJ and ; marked retrograde activation delay and reentry at the previously blocked PMJ. The proposed mechanisms for these events are that reflection across the PMJ generates a premature stimulus that subsequently initiates reentry, where as time-dependent reduction of action potential amplitude, mediated by recovery of the early outward current, causes PMJ conduction block and the subsequent development of reentry following a postmature stimulus. Conduction block at the PMJ during attempted anterograde conduction is caused by the large electrical load, or sink to the large source generated by muscle. Drugs and neurotransmitters that alter the relationship between source and sink may facilitate or suppress reentry accordingly. Further experiments will test the hypothesis that sustained Purkinje-muscle reentry represents a biological oscillator whose period can be advanced, delayed, entrained or annihilated by properly timed subthreshold stimuli delivered to the PMJ. Phase plane trajectories of the reentry circuit will be analyzed to gain insights concerning the nonlinear behavior of reentry. These studies promise to define the mechanisms by which reentry is initiated and sustained and to suggest new ways whereby reentry can be modified.