Key result
Acetylcholine-induced fibrillation transiently increases K efflux ~172% and drives profound Na influx versus control.
Population
Atrial tissue model (specific animal or tissue source not stated in abstract)
Comparison
Acetylcholine (ACh) induced fibrillation vs Control state, ACh alone, or stimulation alone
Design
Preclinical
Authors
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Transient K/Na flux surges in ACh-induced atrial fibrillation do not inform clinical management; leaves open distinct initiation versus maintenance mechanisms.
Absolute Event Rate: 9.37% vs 3.45%
Acetylcholine and fibrillation transiently increase the transmembrane flux of Na and K, suggesting that the initiation and maintenance of atrial fibrillation are governed by separate physicochemical processes.
Klein et al. (1958) studied Atrial Fibrillation. Acetylcholine (ACh) induced fibrillation vs. Control (mean atrial rate of 160/min) was evaluated on K efflux (pmole/cm2sec). Acetylcholine-induced fibrillation transiently increased K efflux from 3.45 to 9.37 pmole/cm2sec and increased Na influx 10-15 times compared to control.
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