Circus movement in rabbit atrial muscle as a mechanism of tachycardia. II. The role of nonuniform recovery of excitability in the occurrence of unidirectional block, as …

MA Allessie, FI Bonke, FJ Schopman - Circulation research, 1976 - Am Heart Assoc
MA Allessie, FI Bonke, FJ Schopman
Circulation research, 1976Am Heart Assoc
Periods of tachycardia were induced in isolated segments (15 X 15 mm) of rabbit left atrium
by local application of a properly timed premature stimulus. We used a special device for
multiple synchronous microelectrode recordings of responses of more than 100 fibers during
the initiation of tachycardia. We clearly demonstrated circus movement of the impulse
through a small area of atrial muscle as the underlying mechanism. The premature impulse
was conducted antegrade in only one direction, whereas in the other directions antegrade …
Periods of tachycardia were induced in isolated segments (15 X 15 mm) of rabbit left atrium by local application of a properly timed premature stimulus. We used a special device for multiple synchronous microelectrode recordings of responses of more than 100 fibers during the initiation of tachycardia. We clearly demonstrated circus movement of the impulse through a small area of atrial muscle as the underlying mechanism. The premature impulse was conducted antegrade in only one direction, whereas in the other directions antegrade conduction failed. The local responses of the fibers in the blocked area served as a temporary obstacle for return of the premature impulse. When these fibers recovered their excitability before extinction of the premature impulse, they were reentered in a retrograde direction, and the impulse traveled in a circular route. During the propagation of a premature beat, local block, which set the stage for circus movement, was caused by nonuniform recovery of excitability of the atrium. We related the spread of activation of a premature impulse to the naturally occurring spatial dispersion in refractory periods and found that local conduction block invariably was associated with an area of delayed restoration of excitability. Artificial induction of differences in refractory periods by regional application of carbamylcholine made it clear that a disparity in refractory periods of only 11-6 msec between adjacent areas may be sufficient to cause local conduction block of a properly timed premature impulse.
Am Heart Assoc