Sodium alterations in isolated rat heart during cardioplegic arrest.

Triple-quantum-filtered (TQF) Na nuclear magnetic resonance (NMR) without chemical shift reagent is used to investigate Na derangement in isolated crystalloid perfused rat hearts during St. Thomas cardioplegic (CP) arrest. The extracellular Na contribution to the NMR TQF signal of a rat heart is found to be 73 +/- 5%, as determined by wash-out experiments at different moments of ischemia and reperfusion. With the use of this contribution factor, the estimated intracellular Na ([Na+]i) TQF signal is 222 +/- 13% of preischemic level after 40 min of CP arrest and 30 min of reperfusion, and the heart rate pressure product recovery is 71 +/- 8%. These parameters are significantly better than for stop-flow ischemia: 340 +/- 20% and 6 +/- 3%, respectively. At 37 degrees C, the initial delay of 15 min in [Na+]i growth occurs during CP arrest along with reduced growth later (approximately 4.0%/min) in comparison with stop-flow ischemia (approximately 6.7%/min). The hypothermia (21 degrees C, 40 min) for the stop-flow ischemia and CP dramatically decreases the [Na+]i gain with the highest heart recovery for CP (approximately 100%). These studies confirm the enhanced sensitivity of TQF NMR to [Na+]i and demonstrate the potential of NMR without chemical shift reagent to monitor [Na+]i derangements.