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Related Experiment Videos

Calcium-dependent fluorescence transients during ventricular fibrillation.

T Stefenelli1, J Wikman-Coffelt, S T Wu

  • 1Department of Medicine (Cardiology), University of California, San Francisco.

American Heart Journal
|September 1, 1990
PubMed
Summary

Ventricular fibrillation in isolated hearts involves abnormal intracellular calcium ([Ca2+]i) transients, often triggered by premature beats and inotropic agents. Calcium levels remained stable or increased during fibrillation, refuting intracellular hypocalcemia.

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Area of Science:

  • Cardiology
  • Physiology
  • Biochemistry

Background:

  • Ventricular fibrillation (VF) is a life-threatening arrhythmia.
  • Understanding the role of intracellular calcium ([Ca2+]i) dynamics during VF is crucial for developing effective treatments.
  • Inotropic agents and altered calcium levels are known to influence cardiac contractility and rhythm.

Purpose of the Study:

  • To investigate the characteristics of calcium transients during experimentally induced ventricular fibrillation in isolated rat and hamster hearts.
  • To determine the intracellular calcium ([Ca2+]i) levels during VF and their relationship with arrhythmogenic triggers.
  • To differentiate patterns of calcium transients associated with different types of VF.

Main Methods:

  • Surface fluorometry using INDO 1-AM was employed to measure calcium-dependent fluorescence transients.

Related Experiment Videos

  • Isolated perfused rat and hamster hearts were subjected to various pro-arrhythmic conditions, including inotropic agent pretreatment and elevated perfusate calcium.
  • Ventricular fibrillation was induced, and calcium transients were recorded during the arrhythmia.
  • Main Results:

    • Thirteen instances of VF occurred in 203 studies, often following pretreatment with agents like isoproterenol, dobutamine, norepinephrine, phenylephrine, digoxin, or high calcium.
    • Alternans of calcium transients were observed in 3 cases, and premature beats preceded VF in 6 cases, leading to increased [Ca2+]i and stronger contractions.
    • Two distinct VF calcium transient patterns were identified: Type 1 (fast, disorganized, small amplitude) and Type 2 (fast, multiform, polymorphous with amplitude changes).
    • [Ca2+]i remained constant or increased during VF, with no evidence of intracellular hypocalcemia.
    • Isoproterenol pretreatment led to end-diastolic [Ca2+]i levels, while other agents/conditions resulted in end-systolic [Ca2+]i levels.

    Conclusions:

    • Premature beats can trigger VF by increasing [Ca2+]i, leading to enhanced subsequent contractions.
    • Distinct patterns of intracellular calcium transients characterize different forms of ventricular fibrillation.
    • Inotropic agents that do not significantly elevate cyclic adenosine monophosphate appear to maintain higher intracellular calcium levels during fibrillation.