Yoriaki Matsumoto

Influence of sympathetic nerve activity on ventricular arrhythmogenicity in the dog with chronic hypokalemia

To examine the influence of sympathetic nerve activity on ventricular arrhyth mogenicity in the dog with chronic hypokalemia, an electrophysiologic study was performed before and after bilateral stellectomy (BS) in 10 dogs with chronic hypokalemia (2.8 ± 0.1 mEq/L), which was created by feeding a low-potassium diet and by administering furosemide over a four-week period, and the results were compared with those obtained from 10 dogs with normokalemia (4.7 ± 0.3 mEq/L) from being fed an ordinary diet over a four-week period. Before BS the incidence of electrically induced ventricular arrhythmias was higher in the hypokalemic than in the normokalemic dogs. After BS it was decreased considerably in the hypokalemic but not in the normokalemic dogs. Heterogeneity of effective refractory period (ΔERP), which was determined as the difference between the longest and shortest effective refractory periods in three sites of the right and left ventricles, was greater in the hypokalemic than in the normokalemic dogs before BS. The ΔERP decreased slightly in the two groups both before and after BS. There was, however, no significant difference in ΔERP in the two groups both before and after BS. Ventricular fibrillation threshold (VFT) was significantly lower in the hypokalemic dogs than in the nor mokalemic dogs before BS (p< 0.005). VFT was elevated in the two groups after BS. Percent increase in VFT after BS was significantly greater in the hypoka lemic than in the normokalemic dogs. In conclusion, sympathetic nerve activity may play an important role in the increase in ventricular arrhythmogenicity in the presence of chronic hypokalemia.

Effect of Bilateral Stellectomy on Electrical Instability of the Atrium in the Dog with Hypokalemia

To investigate the effect of sympathetic nerve activity on electrical instability of the atrium in the presence of hypokalemia, open chest elecfrophysiological study was performed before and after bilateral stellectomy (BS) in 15 dogs with hypokalemia (hypokalemia group) and in 15 dogs with normo‐kalemia (control group). Hypokalemia was created by infusion of 5.0 g/kg of polystyrene sulfonic acid calcium into the colon. Serum level of potassium was significantly lower in the hypokalemia group (2.94 ± 0.52 mEq/L) than in the control group (4.86 ± 0.51 mEq/L, P < 0.01) before BS. There was no significant change in serum level of potassium in the two groups after BS. Incidence of electrically induced atrial fibrillation (AF) was significantly higher in the hypokalemia group (80%) than in the control group (13%, P < 0.001) before BS. It was significantly reduced in (he hypokalemia group (40%, P < 0,05), but not in the control group (6%) after BS. Dispersion of effective refractory period of the atrium (AEHP) was significantly greater in the hypokalemia group (26.1 ± 2.8 msec) than in the control group (22.0 ± 3.3 msec, P < 0.005) before BS. ft was significantly decreased to 23.1 ± 3.2 msec in the hypokalemia group (P < 0.001) and to 20.6 ± 2.5 msec in the control group (P < 0.01) after BS. Maximum conduction delay in the atrium (MaxCD) was 36.1 ± 3.5 msec before and 36.2 ± 4.1 msec after BS in the hypokalemia group and 31.1 ± 4.2 msec before and 32.3 ± 4.9 msec after BS in the control group. There was a significant difference in MaxCD betiveen the two groups before BS. Atrial fibrillation threshold (AFT) was significantly lower in the hypokalemia group (3.9 ± 0.7 mA) than in the control group (33.8 ± 3.1 mA, P < 0.001) before BS. It was significantly increased both in the hypokalemia group (6.5 ± 1.3 mA, P < 0.001) and in the control group (15.0 ± 2.7 mA, P < 0.005) after BS. It is concluded that sympathetic nerve activity may play some role in the increase in electrical instability of the atrium in the presence of hypokalemia.

Effect of verapamil directly administered into A-V node artery on A-V junctional automaticity and A-V conduction in dogs.

Summary: We investigated the direct effects of verapamil, which was infused into the A-V node artery at two doses of 0.01 and 0.1 μg/kg/min on the A-V conduction and the A-V junctional automaticity in the dog with experimentally induced A-V junctional rhythm. Verapamil significantly prolonged the A-H interval, but not the H-V interval, in the His bundle electrogram during atrial pacing at a rate of 100 beats/min. Effective and functional refractory periods of the A-V node also were prolonged significantly by verapamil. On the other hand, verapamil showed less propensity to decrease the spontaneous A-V junctional rate and to prolong the A-V junctional recovery time after atrial overdrive at a rate of 100 beats/min for 60 s. These results indicate that suppressive effects of verapamil on the A-V junctional automaticity are much weaker when compared with that on the A-V conduction.