ABSTRACT
In the present study isolated rat hearts were perfused with calcium free media for 2,4,6,8, and 10 minutes followed by calcium repletion 86Rb+ efflux, protein leakage, percentage rise in resting tension and recovery of developed tension were evaluated. Mechanical activity was not lost completely when calcium was deprived for periods less than 6 minutes, however, readmission of calcium was accompanied by reduction of contractile recovery and 86Rb+ loss. Calcium depletion for a longer periods produced, on calcium readmission, loss of mechanical activity, 86Rb+ and protein loss. A dissociation between some of the indices of the calcium paradox is being shown in this study. The magnitude of contracture does not parallel 86Rb+ efflux and protein loss. In many experimental studies only one or tow indices are used, the assumption being made is that these are sufficient to define the extent of cell damage. This assumption may be dangerous as these indices are not necessarily parallel. Hypothermia and a low calcium concentration perfusion during, the calcium deprivation period, protected the heart against calcium paradox-induced damage and prevented 86Rb+ and protein loss. 86Rb+efflux is suggested here as an alternative index of calcium paradox as it is sensitive and reflects of cell damage