Low sodium attenuation of the Ca2+ paradox in the newborn rabbit myocardium.

The effect of low sodium (Na 24 mM) perfusate during Ca2+ depletion on mechanical function, tissue high-energy phosphate, creatine kinase (CK) release, and tissue potassium was studied in the arterially perfused newborn and adult rabbit heart. During Ca2+ depletion, the time for DT and +dT/dtmax to decline to half-maximal value in newborn muscles perfused with low Na (46 +/- 3 S) was significantly (P less than 0.05) longer than the value obtained with normal Na (14 +/- 1 S). Similar values were obtained in the adult. During Ca2+ repletion, the increase in resting tension and CK release was attenuated in the low Na groups, and the values in the newborn were significantly less than in the adult. The recovery of +dT/dtmax and tissue high-energy phosphates in the low Na groups were significantly greater than in the normal Na groups, and the values in the newborn were significantly greater than in the adult. These data suggest that low Na during the Ca2+-free period delays both cellular Ca2+ depletion during the Ca2+-free period and Ca2+ influx during Ca2+ repletion. This effect in the newborn is greater than in the adult and might be explained by Na+-Ca2+ exchange.