Characteristics of extracellular sodium relaxation in perfused hearts with pathologic interventions.
Sodium spectroscopy and imaging sequences designed to emphasize fast T2 decay or the multiple quantum signal have previously demonstrated a high contrast between normal and pathologic tissue which may be due to changes in intracellular versus extracellular sodium distribution. Since alterations in the amount of signal with fast T2 decay have previously been shown to occur with changes in intracellular sodium content, this study investigated the fast T2 relaxation characteristics of extracellular sodium during pathologic interventions on nonsubmerged perfused rat hearts. T2 data on total sodium content were obtained while global ischemia (stopping all perfusate flow) and extracellular edema (due to long perfusion times) were induced in the heart. The data were fit to a biexponential, with Mf(T2f) the magnitude (time constant) of the fast component of decay. Mf increased significantly in both pathologies (to 319 +/- 26%, n = 3, of baseline for ischemia and to 527 +/- 284%, n = 3, of baseline for edema); the increase with edema was demonstrated to be due to extracellular sodium by intermittently perfusing the heart for a short period with shift reagent. When shift reagent was not used until the conclusion of the edema experiment, Mf increased to 169 +/- 35% of baseline, also due mainly to extracellular sodium. T2f did not exhibit any trends with these experiments, with values ranging from 1.7 to 5.5 ms. We believe that these results indicate that compartmental sodium content will most likely not be quantifiable in pathologic states in the heart with relaxation-based techniques. However, correlations between the pathologic state of the tissue and the sodium NMR signal obtained with pulse sequences or images that emphasize a particular aspect of relaxation may prove to be useful.
Foy
B D
BD
Department of Radiology, Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.
Burstein
D
D
D000818:Animals; D002021:Buffers; D002118:Calcium / Q000008:administration & dosage / Q000493:pharmacokinetics; D002314:Cardioplegic Solutions; D004489:Edema, Cardiac / Q000378:metabolism* / Q000473:pathology; D005110:Extracellular Space / Q000378:metabolism*; D005947:Glucose; D007424:Intracellular Fluid / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000008:administration & dosage / Q000493:pharmacokinetics*; D013997:Time Factors; D014325:Tromethamine
D002021:Buffers; D002314:Cardioplegic Solutions; C074097:Krebs-Henseleit solution; D014325:Tromethamine; D012964:Sodium; D005947:Glucose; D002118:Calcium