Virtual electrodes and the induction of fibrillation in Langendorff-perfused rabbit ventricles: The role of intracellular calcium

Hideki Hayashi, Shien Fong Lin, Boyoung Joung, Hrayr S. Karagueuzian, James N. Weiss, Peng Sheng Chen

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

A strong premature electrical stimulus (S2) induces both virtual anodes and virtual cathodes. The effects of virtual electrodes on intracellular Ca2+ concentration ([Ca2+]i) transients and ventricular fibrillation thresholds (VFTs) are unclear. We studied 16 isolated, Langendorff-perfused rabbit hearts with simultaneous voltage and [Ca 2+]i optical mapping and for vulnerable window determination. After baseline pacing (S1), a monophasic (10 ms anodal or cathodal) or biphasic (5 ms-5 ms) S2 was applied to the left ventricular epicardium. Virtual electrode polarizations and [Ca 2+]i varied depending on the S2 polarity. Relative to the level of [Ca2+]i during the S1 beat, the [Ca2+]i level 40 ms after the onset of monophasic S2 increased by 36 ± 8% at virtual anodes and 20 ± 5% at virtual cathodes (P < 0.01), compared with 25 ± 5% at both virtual cathode-anode and anodecathode sites for biphasic S2. The VFT was significantly higher and the vulnerable window significantly narrower for biphasic S2 than for either anodal or cathodal S 2 (n = 7, P < 0.01). Treatment with thapsigargin and ryanodine (n = 6) significantly prolonged the action potential duration compared with control (255 ± 22 vs. 189 ± 6 ms, P < 0.05) and eliminated the difference in VFT between monophasic and biphasic S2, although VFT was lower for both cases. We conclude that virtual anodes caused a greater increase in [Ca2+]i than virtual cathodes. Monophasic S2 is associated with lower VFT than biphasic S2, but this difference was eliminated by the inhibition of the sarcoplasmic reticulum function and the prolongation of the action potential duration. However, the inhibition of the sarcoplasmic reticulum function also reduced VFT, indicating that the [Ca2+]i dynamics modulate, but are not essential, to ventricular vulnerability.

Original languageEnglish
Pages (from-to)H1422-H1428
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume295
Issue number4
DOIs
Publication statusPublished - 2008 Oct 1

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Electrodes
Rabbits
Calcium
Ventricular Fibrillation
Sarcoplasmic Reticulum
Action Potentials
Ryanodine
Thapsigargin
Pericardium

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Hayashi, Hideki ; Lin, Shien Fong ; Joung, Boyoung ; Karagueuzian, Hrayr S. ; Weiss, James N. ; Chen, Peng Sheng. / Virtual electrodes and the induction of fibrillation in Langendorff-perfused rabbit ventricles : The role of intracellular calcium. In: American Journal of Physiology - Heart and Circulatory Physiology. 2008 ; Vol. 295, No. 4. pp. H1422-H1428.
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abstract = "A strong premature electrical stimulus (S2) induces both virtual anodes and virtual cathodes. The effects of virtual electrodes on intracellular Ca2+ concentration ([Ca2+]i) transients and ventricular fibrillation thresholds (VFTs) are unclear. We studied 16 isolated, Langendorff-perfused rabbit hearts with simultaneous voltage and [Ca 2+]i optical mapping and for vulnerable window determination. After baseline pacing (S1), a monophasic (10 ms anodal or cathodal) or biphasic (5 ms-5 ms) S2 was applied to the left ventricular epicardium. Virtual electrode polarizations and [Ca 2+]i varied depending on the S2 polarity. Relative to the level of [Ca2+]i during the S1 beat, the [Ca2+]i level 40 ms after the onset of monophasic S2 increased by 36 ± 8{\%} at virtual anodes and 20 ± 5{\%} at virtual cathodes (P < 0.01), compared with 25 ± 5{\%} at both virtual cathode-anode and anodecathode sites for biphasic S2. The VFT was significantly higher and the vulnerable window significantly narrower for biphasic S2 than for either anodal or cathodal S 2 (n = 7, P < 0.01). Treatment with thapsigargin and ryanodine (n = 6) significantly prolonged the action potential duration compared with control (255 ± 22 vs. 189 ± 6 ms, P < 0.05) and eliminated the difference in VFT between monophasic and biphasic S2, although VFT was lower for both cases. We conclude that virtual anodes caused a greater increase in [Ca2+]i than virtual cathodes. Monophasic S2 is associated with lower VFT than biphasic S2, but this difference was eliminated by the inhibition of the sarcoplasmic reticulum function and the prolongation of the action potential duration. However, the inhibition of the sarcoplasmic reticulum function also reduced VFT, indicating that the [Ca2+]i dynamics modulate, but are not essential, to ventricular vulnerability.",
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Virtual electrodes and the induction of fibrillation in Langendorff-perfused rabbit ventricles : The role of intracellular calcium. / Hayashi, Hideki; Lin, Shien Fong; Joung, Boyoung; Karagueuzian, Hrayr S.; Weiss, James N.; Chen, Peng Sheng.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 295, No. 4, 01.10.2008, p. H1422-H1428.

Research output: Contribution to journalArticle

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AU - Hayashi, Hideki

AU - Lin, Shien Fong

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