Cl³⁶ and Ca⁴⁵ exchange in atrial fibrillation

¹ Department of Pharmacology, University of Mississippi Medical Center, Jackson, Mississippi

Transmembrane fluxes of Ca⁴⁵ and Cl³⁶ have been investigated during treatment with acetylcholine (ACh), rapid stimulation (1200/min.) and ACh induced fibrillation. Resting Ca⁴⁵ influx was estimated to be 0.024 pmole cm^–2sec^–1. ACh had no effect. Stimulation for 2 hours increased influx to 0.035 pmole cm^–2sec^–1. After 2 hours fibrillation influx reached 0.050 pmole cm^–2sec^–1. The various conditions had no effect on the rate of emergence of Ca⁴⁵. Absolute Cl³⁶ influx in spontaneously beating preparations was estimated to be 1.74 pmole cm^–2sec^–1. Stimulation for 20 minutes increased influx to 3.26 pmole cm^–2sec^–1. After fibrillation (20 min.) influx increased to 4.29 pmole cm^–2sec^–1. Cl³⁶ efflux in controls was estimated to be 1.61 pmole cm^–2sec^–1. After 20 minutes stimulation and fibrillation, the values reached 3.09 and 3.05 pmoles cm^–2sec^–1, respectively. ACh had no effects on either influx or efflux. A comparison of Na, K, Ca and Cl fluxes were made. Data have been interpreted to mean that fibrillation is the result of, or is accompanied by. a marked increase in inward movement of sodium.

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