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Related Experiment Videos

Ca2+ waves during triggered propagated contractions in intact trabeculae

M Miura1, P A Boyden, H E ter Keurs

  • 1Department of Medicine, University of Calgary, Alberta, Canada.

The American Journal of Physiology
|February 12, 1998
PubMed
Summary

Octanol inhibits triggered propagated contractions (TPCs) in cardiac muscle by reducing gap junction permeability, not intracellular calcium release. This finding clarifies how TPCs propagate through heart tissue.

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Area of Science:

  • Cardiovascular Physiology
  • Cellular Electrophysiology
  • Pharmacology

Background:

  • Triggered propagated contractions (TPCs) initiate in damaged cardiac regions and spread through multicellular preparations.
  • Octanol is known to inhibit TPCs, but its precise mechanism of action on calcium signaling and cell-to-cell communication is unclear.

Purpose of the Study:

  • To investigate the effect of octanol on intracellular calcium concentration ([Ca2+]i) dynamics during TPCs.
  • To determine octanol's impact on gap junction permeability (PGJ) in rat cardiac trabeculae.

Main Methods:

  • Measured intracellular Ca2+ concentration ([Ca2+]i) using fura 2 and an image-intensified charge-coupled device camera.
  • Calculated PGJ by assessing fura 2 diffusion coefficients in trabeculae (Dtrab) and myoplasm (Dmyop) after octanol exposure.

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  • Quantified TPC propagation velocity.

    • Main Results:

    • Octanol (100 microM) significantly reduced Dtrab, indicating decreased gap junction permeability.
    • PGJ decreased significantly after 1- and 3-h octanol superfusion.
    • No significant changes in myoplasmic diffusion (Dmyop) were observed, suggesting intracellular calcium diffusion was unaffected.
    • TPC propagation velocity averaged 1.69 +/- 1.48 mm/s.

    Conclusions:

    • Octanol's inhibition of TPCs is primarily mediated by reduced gap junction permeability, affecting intercellular calcium diffusion.
    • TPCs are initiated in damaged areas and propagate via calcium-induced calcium release (CICR) and intercellular gap junction communication.