Abstract
Na2EDTA, when added to isolated toad or rat hearts to give a final concentration of 4 mM, rapidly produced mechanical standstill. If the addition of Na2EDTA was slow, arrhythmias preceded the onset of mechanical quiescence. Provided that the duration of the EDTA perfusion was limited (1 minute), the mechanical depression was reversible. On washing out the Na2EDTA enriched perfusate, arrhythmias (including fibrillation) were recorded. These arrhythmias developed both in the presence and in the absence of electrical stimulation. Subsequently a brief period of mechanical potentiation ensued. Lesser concentrations of Na2EDTA (1 mM) induced arrhythmias which were independent of mechanical arrest.
It is concluded that Na2EDTA chelates sonic of the Ca++ located in the cell membrane and in so doing may cause the onset of spontaneous activity including fibrillation.
Footnotes
- Received February 9, 1962.
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