K+ and Mg-2+ net fluxes in relation to zero [Ca-2+] perfusion and subsequent cardiac contracture.

Following within 45 sec after the development of contracture induced by restoring normal ionic composition perfusion conditions after a 12 min period of mechanical arrest in the rabbit heart caused by zero [Ca-2+] perfusion, there is an explosive efflux of K+ and Mg-2+. After shorter periods of Ca-2+-lack arrest, the restoration of [Ca-2+] to normal causes recovery of rhythmic contraction and no K+ efflux. The K+ and Mg-2+ effuxes are ascribed to the effects of the contracture itself and not simply to the loss of Ca-2+ during zero [Ca-2+] arrest nor to the restoration of normal perfusate [Ca-2+], except insofar as the latter operates to induce the contracture. It is suggested that cell membrane permeability progressively increases during zero [Ca-2+] arrest and that an abnormally large influx of Ca-2+ after restoration of normal perfusate [Ca-2+] induces the contracture.