23Na and 31P nuclear magnetic resonance studies of ischemia-induced ventricular fibrillation: Alterations of intracellular Na+ and cellular energy

Martin Pike, C. S. Luo, S. Yanagida, G. R. Hageman, P. G. Andersen

Research output: Contribution to journalArticle

38 Citations (Scopus)

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 aorticbanded (band) rats (P+ 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+-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.

Original languageEnglish (US)
Pages (from-to)394-406
Number of pages13
JournalCirculation Research
Volume77
Issue number2
StatePublished - Aug 1995
Externally publishedYes

Fingerprint

Ventricular Fibrillation
Magnetic Resonance Spectroscopy
Ischemia
Phosphates
Maintenance

Keywords

  • Cardiac hypertrophy
  • Intracellular Na
  • Ischemia
  • Nuclear magnetic resonance
  • Ventricular fibrillation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

23Na and 31P nuclear magnetic resonance studies of ischemia-induced ventricular fibrillation : Alterations of intracellular Na+ and cellular energy. / Pike, Martin; Luo, C. S.; Yanagida, S.; Hageman, G. R.; Andersen, P. G.

In: Circulation Research, Vol. 77, No. 2, 08.1995, p. 394-406.

Research output: Contribution to journalArticle

@article{8ec2b651ecef456786318cddfeb812b7,
title = "23Na and 31P nuclear magnetic resonance studies of ischemia-induced ventricular fibrillation: Alterations of intracellular Na+ and cellular energy",
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 aorticbanded (band) rats (P+ 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+-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.",
keywords = "Cardiac hypertrophy, Intracellular Na, Ischemia, Nuclear magnetic resonance, Ventricular fibrillation",
author = "Martin Pike and Luo, {C. S.} and S. Yanagida and Hageman, {G. R.} and Andersen, {P. G.}",
year = "1995",
month = "8",
language = "English (US)",
volume = "77",
pages = "394--406",
journal = "Circulation Research",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - 23Na and 31P nuclear magnetic resonance studies of ischemia-induced ventricular fibrillation

T2 - Alterations of intracellular Na+ and cellular energy

AU - Pike, Martin

AU - Luo, C. S.

AU - Yanagida, S.

AU - Hageman, G. R.

AU - Andersen, P. G.

PY - 1995/8

Y1 - 1995/8

N2 - 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 aorticbanded (band) rats (P+ 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+-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.

AB - 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 aorticbanded (band) rats (P+ 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+-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.

KW - Cardiac hypertrophy

KW - Intracellular Na

KW - Ischemia

KW - Nuclear magnetic resonance

KW - Ventricular fibrillation

UR - http://www.scopus.com/inward/record.url?scp=0028990887&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028990887&partnerID=8YFLogxK

M3 - Article

C2 - 7614723

AN - SCOPUS:0028990887

VL - 77

SP - 394

EP - 406

JO - Circulation Research

JF - Circulation Research

SN - 0009-7330

IS - 2

ER -