APStracts 3:0405A, 1996.

Sodium alterations in isolated rat heart during cardioplegic arrest. Schepkin, V. D., I. O. Choy, T. F. Budinger. Center for Functional Imaging, Lawrence Berkeley National Laboratory, Berkeley, CA 94720.

APStracts 3:0405A, 1996.

Triple-quantum filtered (TQF) sodium NMR without chemical shift reagent is used to investigate sodium derangement in isolated crystalloid perfused rat hearts during St. Thomas cardioplegic arrest (CP). The extracellular sodium contribution to the NMR TQF signal of a rat heart is found to be 73 +/- 5%, determined by wash out experiments at different moments of pre-ischemia and reperfusion. Using this contribution factor the estimated intracellular sodium TQF signal is 222 +/- 13% of pre-ischemic level after 40 min of CP arrest and 30 min of reperfusion, 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 C the initial delay of 15 min in intracellular sodium growth occurs during CP arrest along with reduced growth later (4.0 %/min) in comparison to stop-flow ischemia (6.7 %/min). The hypothermia (21 C, 40 min) for the stop-flow ischemia and cardoplegic arrest dramatically decreases the intracellular sodium gain with the highest heart recovery for CP (100%). These studies confirm the enhanced sensitivity of TQF NMR to intracellular sodium and demonstrate the potential of NMR without chemical shift reagent to monitor intracellular sodium derangements.

Received 16 January 1996; accepted in final form 12 August 1996.
APS Manuscript Number A53-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996