Two-dimensional In Vivo Experiments
نویسندگان
چکیده
We have found that when suprathreshold cathodal stimuli were applied to the epicardium of canine ventricle, impulse propagation originated at a "virtual cathode" with dimensions greater than those of the physical cathode. We report the two-dimensional geometry of the virtual cathode as a function of stimulus strength; the results are compared with the predictions of an anisotropic, bidomain model of cardiac conduction recently developed in our laboratories. Data were collected in six pentobarbital-anesthetized dogs by using a small plaque electrode sewn to the left ventricular epicardium. Arrival times at closely spaced bipolar electrodes oriented radially around a central cathode were obtained as a function of stimulus strength and fiber orientation. The dimensions of the virtual cathode were determined by linear backextrapolation of arrival times to the time of stimulation. The directional dependence of the conduction velocity was consistent with previous reports: at 1 mA, longitudinal (00) and transverse (90°) velocities were 0.60±0.03 and 0.29+±0.02 m/sec, respectively. At 7 mA, the longitudinal velocity was 0.75+±0.05 m/sec, whereas there was no significant change in the transverse velocity. In contrast to conduction velocity, the virtual cathode was smallest in the longitudinal orientation and largest between 45° and 600. Virtual cathode size was dependent on both orientation and stimulus strength: at 00, the virtual cathode was small (-1 mm) and relatively constant over the range of 1-7 mA; at oblique orientations (45°-90°), it displayed a roughly logarithmic dependence on stimulus strength, -1 mm at 1 mA and -3 mm at 7 mA. The bidomain, anisotropic model reproduced both the stimulus strength and the fiberorientation dependence of the virtual cathode geometry when the intracellular and extracellular anisotropies were 10: 1 and 4: 1, respectively, but not when the two anisotropies were equal. We suggest that the virtual cathode provides a direct measure of the determinants of cardiac activation; its complex geometry appears to reflect the bidomain, anisotropic nature of cardiac muscle. (Circulation Research 1991;68:513-530)
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