Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

BACKGROUND: Ventricular fibrillation has deleterious metabolic and functional consequences for the heart. This study had two purposes: first, to define the effects of ventricular fibrillation during hypoxia on energy metabolism and accumulation of intracellular Na+ and, second, to test whether the occurrence of ventricular fibrillation can be predicted from functional or metabolic parameters. METHODS AND RESULTS: Isolated isovolumic rat hearts were perfused with oxygenated Krebs-Henseleit buffer at 37 degrees C. After a prehypoxic period, hearts were subjected to hypoxic perfusion (95% N2-5% CO2) for 30 minutes. High-energy phosphates and intracellular pH were determined by 31P-nuclear magnetic resonance (NMR) spectroscopy, and intracellular Na+ accumulation was followed by 23Na-NMR spectroscopy in combination with the shift reagent dysprosium triethylenetetraminehexa-acetate. Five of 10 (31P-NMR) and four of 10 (23Na-NMR) hearts developed spontaneous ventricular fibrillation at 19 +/- 2 minutes (31P-NMR) and 18 +/- 3 minutes (23Na-NMR) of hypoxia (ventricular fibrillation group), whereas other hearts (non-ventricular fibrillation group) remained beating throughout hypoxia. Cardiac function and high-energy phosphate content declined during hypoxia, and ventricular fibrillation exacerbated this decline significantly. Similarly, ventricular fibrillation exacerbated the accumulation of intracellular Na+ occurring during hypoxia. Statistical analysis showed that the event of ventricular fibrillation could be predicted from changes of end-diastolic pressure, rate-pressure product, and creatine phosphate content before ventricular fibrillation. However, the strongest predictor of ventricular fibrillation was intracellular Na+ accumulation, which occurred in ventricular fibrillation hearts throughout the hypoxic period long before ventricular fibrillation was initiated. CONCLUSIONS: Loss of systolic and diastolic functions, creatine phosphate depletion, and, in particular, intracellular Na+ accumulation may be causally related to induction of ventricular fibrillation during hypoxia, all of which are most likely linked to concomitant intracellular Ca2+ accumulation.

Type

Journal article

Journal

Circulation

Publication Date

07/1992

Volume

86

Pages

302 - 310

Keywords

Adenosine Triphosphate, Animals, Blood Pressure, Forecasting, Heart Rate, Hypoxia, In Vitro Techniques, Intracellular Membranes, Magnetic Resonance Spectroscopy, Male, Myocardium, Phosphorus, Rats, Rats, Inbred Strains, Sodium, Ventricular Fibrillation