OBJECTIVE: The aim was to examine under abnormal conditions the flow of currents across junctional (J-) cells found between Purkinje fibre cells and ventricular muscle cells, and determine whether these currents play a role in increasing the excitation rate of ventricular muscle. METHODS: Canine Purkinje fibre and papillary muscle preparations were mapped to locate the Purkinje fibre-ventricular muscle cell junction (PVJ). Using standard techniques, action potentials from Purkinje fibres, J-cells, and ventricular muscle cells and extracellular electrograms were simultaneously recorded at the PVJ. The tissue was then superfused with Tyrode solution plus 4.5-5.0 mmol of ethylenediamine tetra-acetate (EDTA). RESULTS: EDTA prolonged the action potential duration mainly in Purkinje fibres. Secondary plateaus were recorded at membrane potentials of -63.5(SD 7.6) mV (n = 16) in J-cells, and at membrane potentials of -74.9(4.3) mV (n = 9) in ventricular muscle cells. Triggered activations appeared on both secondary plateaus with the earliest site of activation at J-cells (n = 12), at ventricular muscle cells (n = 4), or in both (n = 6). Tetrodotoxin (3-9 x 10(-7) M) and verapamil (1 x 10(-6)-10(-5) M) suppressed triggered activations. CONCLUSION: The PVJ zone appears to be an important site for the generation of triggered activations. Interventions suggest that triggered activations originating in the J-cell depend on delayed repolarisations which trigger the activation of sodium and/or calcium channels.
OBJECTIVE: The aim was to examine under abnormal conditions the flow of currents across junctional (J-) cells found between Purkinje fibre cells and ventricular muscle cells, and determine whether these currents play a role in increasing the excitation rate of ventricular muscle. METHODS:Canine Purkinje fibre and papillary muscle preparations were mapped to locate the Purkinje fibre-ventricular muscle cell junction (PVJ). Using standard techniques, action potentials from Purkinje fibres, J-cells, and ventricular muscle cells and extracellular electrograms were simultaneously recorded at the PVJ. The tissue was then superfused with Tyrode solution plus 4.5-5.0 mmol of ethylenediamine tetra-acetate (EDTA). RESULTS:EDTA prolonged the action potential duration mainly in Purkinje fibres. Secondary plateaus were recorded at membrane potentials of -63.5(SD 7.6) mV (n = 16) in J-cells, and at membrane potentials of -74.9(4.3) mV (n = 9) in ventricular muscle cells. Triggered activations appeared on both secondary plateaus with the earliest site of activation at J-cells (n = 12), at ventricular muscle cells (n = 4), or in both (n = 6). Tetrodotoxin (3-9 x 10(-7) M) and verapamil (1 x 10(-6)-10(-5) M) suppressed triggered activations. CONCLUSION: The PVJ zone appears to be an important site for the generation of triggered activations. Interventions suggest that triggered activations originating in the J-cell depend on delayed repolarisations which trigger the activation of sodium and/or calcium channels.
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