An in vitro preparation of rabbit right atrium, including the A-V node (AVN) and bundle of His, was utilized to evaluate the mechanism of paroxysmal supraventricular tachycardia (SVT). Microelectrode recordings from atrium and AVN were obtained. During sinus rhythm the atrial cycle was explored with atrial premature depolarizations (APD). Fifty episodes of an arrhythmia with characteristics identical to SVT in man were produced in six of 40 rabbits. In vitro, SVT: (1) was initiated by a single APD showing prolonged conduction in the AVN; (2) had initial cycles similar to atrial echoes; (3) in most instances showed 1:1 A-V conduction; (4) lasted 20 to 500 cycles; and (5) could be ended by a single APD which penetrated the AVN. Reentry in the upper AVN was established by the recording of action potentials from nodal cells which showed marked electrotonic "humps" during repolarization. SVT and atrial echoes could not be produced after damaging or sectioning the upper AVN. An in vitro model of SVT supports the hypothesis that this arrhythmia results from reentry within the AVN.