K + and Mg 2+ Net Fluxes in Relation to Zero [Ca 2+ ] Perfusion and Subsequent Cardiac Contracture 1

Abstract

Summary

Following within 45 sec after the development of contracting induced by restoring normal ionic composition per-fusion conditions after a 12 min period of mechanical arrest in the rabbit heart caused by zero [Ca²⁺] perfusion, there is an explosive efflux of K⁺ and Mg²⁺. After shorter periods of Ca²⁺-lack arrest, the restoration of [Ca²⁺] to normal causes recovery of rhythmic contraction and no K⁺ efflux. The K⁺ and Mg²⁺ effluxes are ascribed to the effects of the contracture itself and not simply to the loss of Ca²⁺ during zero [Ca²⁺] arrest nor to the restoration of normal perfusate [Ca²⁺], except insofar as the latter operates to induce the contracture. It is suggested that cell membrane permeability progressively increases during zero [Ca²⁺] arrest and that an abnormally large influx of Ca²⁺ after restoration of normal perfusate [Ca²⁺] induces the contracture.