© 1995 American Heart Association, Inc.
Articles |
23Na and 31P Nuclear Magnetic Resonance Studies of Ischemia-Induced Ventricular Fibrillation
Alterations of Intracellular Na+ and Cellular Energy
From the Department of Medicine (M.M.P., C.S.L., S.Y.), Division of Cardiovascular Disease; the Department of Physiology and Biophysics (G.R.H.); and the Department of Pathology (P.G.A.), Division of Molecular/Cellular Pathology; University of Alabama at Birmingham.
Correspondence to Dr M.M. Pike, Department of Medicine, Division of Cardiovascular Disease, 703 S 19th Street, ZRB 308, Birmingham, AL 35294-0007.
Abstract To clarify the role of
Na+i, pHi, and
high-energy phosphate (HEP) levels in the initiation and
maintenance of ischemia-induced ventricular
fibrillation (VF), interleaved 23Na and 31P
nuclear magnetic resonance spectra were collected on perfused rat
hearts during low-flow ischemia (51 minutes, 1.2 mL/g wet wt).
When untreated, 50% of the hearts from normal (sham) rats and 89% of
the hypertrophied hearts from aortic-banded (band) rats
(P<.01 versus sham) exhibited VF. Phosphocreatine content
was significantly higher in sham than band hearts during control
perfusion (53.3±1.6 versus 39.8±2.0 µmol/g dry wt). Before VF at 20
minutes of ischemia, Na+i accumulation
was greater in hearts that eventually developed VF than in hearts that
did not develop VF for both band and sham groups (144% versus 128% of
control in sham; P<.005) and was the strongest
metabolic predictor of VF; ATP depletion was also greater
for VF hearts in the sham group. Infusion of the
Na+-H+ exchange inhibitor
5-(N,N-hexamethylene)-amiloride prevented
VF in sham and band hearts; reduced Na+i
accumulation but similar HEP depletion were observed compared with VF
hearts before the onset of VF. Rapid changes in
Na+i, pHi, and HEP
began with VF, resulting in intracellular Na+i
overload (
300% of control) and increased HEP depletion. A delayed
postischemic functional recovery occurred in VF hearts,
which correlated temporally with the recovery of
Na+i. In conclusion, alterations in
Na+i were associated with spontaneous VF
transitions, consistent with involvement of excess
Na+i accumulation in VF initiation and
maintenance and with previously reported alterations in
Ca2+i with VF. Hypertrophied band hearts
exhibited enhanced susceptibility to ischemia-induced VF,
possibly linked to a lower HEP reserve.
Key Words: ventricular fibrillation • intracellular Na+ • ischemia • nuclear magnetic resonance • cardiac hypertrophy
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