Circulation, Vol 80, 369-379, Copyright © 1989 by American Heart Association
Y Koretsune and E Marban
The mechanism of ventricular fibrillation is poorly understood at the
cellular level. We explored the role of intracellular free calcium in the
pathophysiology and pathogenesis of ventricular fibrillation in perfused
ferret hearts loaded with the Ca2+ indicator 5F-BAPTA. Nuclear magnetic
resonance spectroscopy was used to measure [Ca2+]i, pH, and high-energy
phosphates. During ventricular fibrillation induced by burst pacing,
[Ca2+]i rose rapidly and dramatically, exceeding by four times the control
within 5 minutes. [Ca2+]i remained markedly elevated throughout 20 minutes
of fibrillation, but it returned to control values shortly after
defibrillation. In a group of hearts kept isovolumic by a balloon in the
left ventricle, acidosis and high-energy phosphate depletion developed
despite the maintenance of normal coronary pressure. To distinguish the
effects of superimposed ischemia from those of the arrhythmia itself, we
lowered left ventricular volume during fibrillation in a second group of
hearts. This maneuver decreased wall stress such that fibrillation had no
significant adverse effect on intracellular pH, high-energy phosphates, or
lactate efflux. [Ca2+]i still increased remarkably despite the absence of
ischemic changes. Developed pressure did not recover to control levels
after defibrillation in either group; the hearts appeared "stunned." We
conclude that intracellular calcium increases as a direct consequence of
ventricular fibrillation. The increase in [Ca2+]i may cause the contractile
dysfunction observed in postarrhythmic hearts. Its possible role in
initiating or maintaining the arrhythmia is less clear.
ARTICLES
Cell calcium in the pathophysiology of ventricular fibrillation and in the pathogenesis of postarrhythmic contractile dysfunction
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
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