23Na and 31P nuclear magnetic resonance studies of ischemia-induced ventricular fibrillation. Alterations of intracellular Na+ and cellular energy
| Autor: | Gilbert R. Hageman, Cameron S. Luo, S. Yanagida, Peter G. Anderson, Martin M. Pike |
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| Rok vydání: | 1995 |
| Předmět: |
High-energy phosphate
Male medicine.medical_specialty Magnetic Resonance Spectroscopy Time Factors Phosphocreatine Physiology Sodium Ischemia Myocardial Ischemia chemistry.chemical_element Cardiomegaly In Vitro Techniques Muscle hypertrophy Rats Sprague-Dawley chemistry.chemical_compound Nuclear magnetic resonance Adenosine Triphosphate Internal medicine medicine Animals Analysis of Variance business.industry Phosphorus Isotopes medicine.disease Rats Perfusion Endocrinology chemistry Ventricular fibrillation Ventricular Fibrillation Lactates Sodium Isotopes Cardiology and Cardiovascular Medicine business Energy Metabolism Intracellular |
| Zdroj: | Circulation research. 77(2) |
| ISSN: | 0009-7330 |
| Popis: | Abstract To clarify the role of Na + i , pH i , and high-energy phosphate (HEP) levels in the initiation and maintenance of ischemia-induced ventricular fibrillation (VF), interleaved 23 Na and 31 P 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 + 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 , pH i , 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 Ca 2+ i with VF. Hypertrophied band hearts exhibited enhanced susceptibility to ischemia-induced VF, possibly linked to a lower HEP reserve. |
| Databáze: | OpenAIRE |
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