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Effect of Bilateral Stellectomy on Electrical Instability of the Atrium in the Dog with Hypokalemia
Author(s) -
YANO KATSUSUKE,
MITSUOKA TAKAO,
HIRATA TETSUYA,
HAND OSAMU,
HIRATA MASANOBU,
MATSUMOTO YORIAKI
Publication year - 1992
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1992.tb06501.x
Subject(s) - hypokalemia , medicine , anesthesia , potassium , endocrinology , organic chemistry , chemistry
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.