Cl36 and Ca45 exchange in atrial fibrillation
- 1 October 1959
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 197 (4) , 752-756
- https://doi.org/10.1152/ajplegacy.1959.197.4.752
Abstract
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.Keywords
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