K+ and Mg2+ Net Fluxes in Relation to Zero [Ca2+] Perfusion and Subsequent Cardiac Contracture 1

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.