Survival of metabolically inhibited ventricular myocytes is enhanced by inhibition of rigor and SR Ca2+ cycling

Treatment with caffeine and 2,3-butanedione monoxime (BDM) markedly protects adult rabbit ventricular myocytes from ATP depletion injury and enhances their long-term survival. BDM prevents contracture, and inhibits both Ca2+ -induced force development and rigor due to ATP depletion. Caffeine prevents the oscillatory release of Ca2+ from sarcoplasmic reticulum. The resting membrane potential normalizes after 24 hrs of metabolic inhibition. However, myocyte functioning shows characteristics of stunning with depression in myocyte contractility and impairment in relaxation.