Na24 and K42 Exchange in Atrial Fibrillation

Abstract

Changes in transmembrane flux of Na²⁴ and K⁴² during acetylcholine (ACh) induced fibrillation have been investigated. At a mean atrial rate of 160/min., the efflux of K was estimated to be 3.45 pmole/cm²sec. With the onset of fibrillation the efflux reached a mean value of 9.37 pmole/cm²sec. This rate was 50% greater than the combined effects of ACh (8.0 x 10^–4 gm/ml) and stimulation (1200/ min.) alone. With the onset of fibrillation a momentary increase of influx followed by a decrease to 1/20–1/40 the control was observed. ACh alone produced comparable effects. The rate of Na influx was increased 10–15 times by both ACh and fibrillation. Similar changes in Na efflux were noted but of a smaller magnitude. The change in fluxes noted are transient in nature with the rate returning rapidly to that of the control even though fibrillation continues. Upon cessation of the arrhythmia a momentary increase of K efflux was again observed. It is concluded that ACh and fibrillation increase the transmembrane flux of Na and K. With the present method the onset of fibrillation is best correlated with an increase of K efflux above a critical rate. Since these changes are transient, it appears that the initiation and maintenance of the arrhythmia are governed by separate physicochemical processes.