To determine the cellular electrophysiological mechanisms for unidirectional conduction block and re-entrant excitation, single cycles of circus movement re-entry were induced in canine Purkinje fibre-papillary muscle preparations containing two Purkinje fibre-muscle junctions (PMJs). The preparations were mounted in a partitioned tissue bath that permitted independent superfusion of each PMJ. The pre-existing dispersion of refractoriness between PMJs was accentuated by superfusing PMJ1 with normal Tyrode solution or Tyrode solution containing 6-8 mM KCl and superfusing PMJ2 with Tyrode solution containing 0.5 mM heptanol and 4-10 mM KCl. 2. Premature stimuli delivered to the Purkinje fibre induced unidirectional anterograde conduction block at PMJ2. Conduction proceeded from Purkinje cells to papillary muscle at PMJ1 and from papillary muscle retrogradely across the previously blocked PMJ2. 3. The difference in refractory periods between the two PMJs defined a range of premature coupling intervals within which re-entry was inducible. Conduction block at the PMJ occurred in papillary muscle at short coupling intervals and in the Purkinje fibre at longer intervals. 4. Once initiated, re-entry could be reset or annihilated by properly timed subthreshold current pulses delivered to cells at the PMJ. 5. To define better the mechanisms for conduction block and re-entry, an analytical model was developed using non-linear regression analysis to derive equations from the experimental results. Varying parameters within the constraints of the model reproduced the key features of the rate-dependent conduction block observed experimentally. Critical elements of the model included the induction of significant activation delays at short diastolic intervals and a reduction in the rate of action potential duration restitution after exposure to heptanol. 6. These results help to establish the conditions necessary for induction of one-dimensional circus movement re-entry and to define the roles of non-linearities of activation delay and excitability in the dynamics of conduction block at the PMJ.
摘要
为了确定单向传导阻滞和折返激动的细胞电生理机制，在含有两个浦肯野纤维 - 乳头肌连接点（PMJ）的犬浦肯野纤维 - 乳头肌标本中诱发了单周期的环形运动折返。将标本安装在分隔的组织浴中，允许对每个PMJ进行独立灌注。通过用正常台氏液或含6 - 8 mM KCl的台氏液灌注PMJ1，并用含0.5 mM庚醇和4 - 10 mM KCl的台氏液灌注PMJ2，增强了PMJ之间预先存在的不应期离散。2. 向浦肯野纤维施加的过早刺激在PMJ2处诱发单向顺向传导阻滞。在PMJ1处，传导从浦肯野细胞传至乳头肌，并从乳头肌逆向穿过先前阻滞的PMJ2。3. 两个PMJ之间不应期的差异定义了一个过早偶联间期范围，在此范围内可诱发折返。在短偶联间期时，PMJ处的传导阻滞发生在乳头肌，而在较长间期时发生在浦肯野纤维。4. 一旦折返启动，通过在PMJ处向细胞施加适时的阈下电流脉冲，可以重置或消除折返。5. 为了更好地定义传导阻滞和折返的机制，使用非线性回归分析开发了一个分析模型，从实验结果中推导方程。在模型的约束范围内改变参数，再现了实验观察到的频率依赖性传导阻滞的关键特征。模型的关键要素包括在短舒张间期诱导显著的激活延迟，以及暴露于庚醇后动作电位时程恢复速率的降低。6. 这些结果有助于确定诱发一维环形运动折返所需的条件，并定义激活延迟和兴奋性非线性在PMJ传导阻滞动力学中的作用。
