Load dependence of ventricular performance explained by model of calcium-myofilament interactions

Juichiro Shimizu, Koji Todaka, Daniel Burkhoff

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Although a simple concept of load-independent behavior of the intact heart evolved from early studies of isolated, intact blood-perfused hearts, more recent studies showed that, as in isolated muscle, the mode of contraction (isovolumic vs. ejection) impacts on end-systolic elastance. The purpose of the present study was to test whether a four-state model of myofilament interactions with length-dependent rate constants could explain the complex contractile behavior of the intact, ejecting heart. Studies were performed in isolated, blood-perfused canine hearts with intracellular calcium transients measured by macroinjected aequorin. Measured calcium transients were used as the driving function for the model, and length-dependent rate constants yielding the highest concordance between measured and model-predicted midwall stress at different isovolumic volumes were determined. These length-dependent rate constants successfully predicted contractile behavior on ejecting contractions. This, along with additional model analysis, suggests that length-dependent changes in calcium binding affinity may not be an important factor contributing to load-dependent contractile performance in the intact heart under physiological conditions.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume282
Issue number3 51-3
Publication statusPublished - Jun 29 2002
Externally publishedYes

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Myofibrils
Calcium
Aequorin
Muscle Contraction
Canidae

All Science Journal Classification (ASJC) codes

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

Cite this

Load dependence of ventricular performance explained by model of calcium-myofilament interactions. / Shimizu, Juichiro; Todaka, Koji; Burkhoff, Daniel.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 282, No. 3 51-3, 29.06.2002.

Research output: Contribution to journalArticle

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