ELECTROPHYSIOLOGY OF RIGHT ATRIAL SUBSIDIARY PACEMAKERS

正常情况下，窦房结(窦房结)起主要起搏器的作用 心之所向。然而，在权利范围内有附属的起搏器 SA节点外的中庭，可用作故障保护机制 在SA节点功能障碍的情况下或可能负责生成 房性心律失常。尽管它们的重要性得到了很好的认识，但很少有 已知辅助心房起搏器的功能。因此，龙 这项研究的范围目标是阐明超微结构， 副心房的电生理和功能特征 起搏器活动。 显示辅助起搏器活动的心房组织从 用戊巴比妥钠(40 mg/kd；iv)麻醉的猫。 标准的细胞内微电极将被用于研究电学 活动和光电位移传感器将用于 测量产生了张力。来研究负责的离子流 辅助起搏器活动，单个起搏器细胞将通过 利用单个全细胞电压进行酶分散和电压钳制 钳夹技术。最后，光学和电子显微镜将被用来 研究辅助起搏器纤维的超微结构特征。 初步结果表明，辅助心房起搏器具有自律性。 主要由钙的运动决定。因此，在第一节中， 提议的细胞内微电极和张力记录将是 用于研究辅助起搏器对特定条件下的反应 通过以下途径改变钙运动的药物和干预措施 1)慢内向电流，2)肌浆内释放 网状结构，3)钠/钙交换，4)钙调素调节 进程。在第二节中，将使用酶分散来分离单个 用于单个全细胞电压钳研究的起搏器细胞。首字母 实验将测试单个细胞的生存能力。电流-电压 关系将被用来确定离子电导特性。 最后，实验将直接用于确定离子电流。 参与辅助起搏器自动起搏器。这些研究将 为加深我们的理解提供新的重要信息 辅助起搏器活动的基本机制。此外, 它们将为房性心律失常的机制提供新的见解。

Normally, the sinoatrial node (SA node) functions as the primary pacemaker of the heart. However, there are subsidiary pacemakers within the right atrium, outside of the SA node, that may function as a failsafe mechanism in the event of SA node dysfunction or may be responsible for generating atrial dysrhythmias. Although their importance is well recognized, little is known about subsidiary atrial pacemaker function. Therefore, the long range goal of this research is to elucidate the ultrastructural, electrophysiological and functional characteristics of subsidiary atrial pacemaker activity. Atrial tissue exhibiting subsidiary pacemaker activity is obtained from cats that are anesthetized with sodium pentobarbital (40 mg/kd; iv). Standard intracellular microelectrodes will be used to study the electrical activity and a photoelectric displacement transducer will be used to measure developed tension. To study the ionic currents responsible for subsidiary pacemaker activity, single pacemaker cells will be obtained by enzymatic dispersion and voltage clamped using single whole cell voltage clamp techniques. Finally, light and electron microscopy will be used to study the ultrastructural characteristics of subsidiary pacemaker fibers. Preliminary results indicate that subsidiary atrial pacemaker automaticity is determined primarily by calcium movements. Therefore, in section I of the proposal intracellular microelectrodes and tension recordings will be used to study the response of subsidiary pacemakers to specific pharmacological agents and interventions that alter calcium movements via 1) the slow inward current, 2) intracellular release from the sarcoplasmic reticulum, 3) sodium/calcium exchange, and 4) a calmodulin regulated process. In section II, enzyme dispersion will be used to isolate single pacemaker cells for single whole cell voltage clamp studies. The initial experiments will test the viability of the single cells. Current-voltage relations will be used to determine ionic conductance characteristics. Finally, experiments will be directed toward determining the ionic currents participating in subsidiary pacemaker automaticity. These studies will provide new and important information toward furthering our understanding of fundamental mechanisms of subsidiary pacemaker activity. In addition, they will provide new insight into mechanisms of atrial dysrhythmias.