MRI of total sodium (Na) content may allow assessment of myocardial viabili
ty, but information on Na content in normal myocardium, necrotic/scar tissu
e, and stunned or hibernating myocardium is lacking. Thus, the aims of the
study were to: 1) quantify the temporal changes in myocardial Na content po
stmyocardial infarction (Mr) in a rat model (Protocol 1); 2) compare Na in
normally perfused, hibernating, and stunned canine myocardium (Protocol 2);
and 3) determine whether, in buffer-perfused rat hearts, infarct scar can
be differentiated from intact myocardium by Na-23-MRI (Protocol 3), In Prot
ocol 1, rats were subjected to LAD ligation. Infarct/scar tissue was excise
d at control and 1, 3, 7, 28, 56, and 128 days post-MI (N = 6-8 each), Na c
ontent was determined by Na-23-NMR spectroscopy (MRS) and ion chromatograph
y. Na content was persistently increased at all time points post-MI averagi
ng 306*-160*% of control values (*P < 0.0083 vs. control). In Protocol 2, N
a-23-MRS of control (baseline), stunned and hibernating samples revealed no
difference in Na. In Protocol 3, 23Na-MRI revealed a mean increase in sign
al intensity, to 142 +/- 6% of control values, in scar tissue. A threshold
of 2 standard deviations of the image intensity allowed determination of in
farct size, correlating with histologically determined infarct size (r = 0.
91, P < 0.0001), (C) 2001 Wiley-Liss, Inc.