Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Myocardial cell energetics

H Kammermeier1

  • 1Institute of Physiology, Faculty of Medicine, RWTH, Aachen, Germany.

Advances in Experimental Medicine and Biology
|January 1, 1997
PubMed
Summary
This summary is machine-generated.

Myocardial energetics are highly efficient, but energy deficiency critically impacts ATP-dependent processes. Interventions affecting calcium and ion cycling alter contraction economy in cardiomyocytes.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Activation of ATP-sensitive potassium channels in hypoxic cardiac failure is not mediated by adenosine-1 receptors in the isolated rat heart.

Journal of cardiovascular pharmacology and therapeutics·2001
Same author

Quantification of horseradish peroxidase delivery into the arterial wall in vivo as a model of local drug treatment: comparison between a porous and a gel-coated balloon catheter.

Cardiovascular and interventional radiology·1999
Same author

Effects of high glucose on the hypoxic isolated guinea pig heart: interactions with ATP-dependent K+ channels?

Biochimica et biophysica acta·1999
Same author

Luminometric measurement of malate and glucose-6-phosphate in mammalian tissue.

Methods in molecular biology (Clifton, N.J.)·1998
Same author

Halothane, but not isoflurane, impairs the beta-adrenergic responsiveness in rat myocardium.

Anesthesiology·1998
Same author

Relation between enzyme release and irreversible cell injury of the heart under the influence of cytoskeleton modulating agents.

Biochimica et biophysica acta·1998
Same journal

Peptidomics in the Spotlight: Advanced Sample Treatment Techniques and Analytical Insights.

Advances in experimental medicine and biology·2026
Same journal

Methods for the Investigation of Protein-Ligands Interactions.

Advances in experimental medicine and biology·2026
Same journal

Sample Preparation Strategies for Microbial Cell Surface Proteomics: Integrating Shaving and Shotgun Approaches.

Advances in experimental medicine and biology·2026
Same journal

Proteomic Sample Preparation for the Petroleum Industry: A Biocorrosion Case Study.

Advances in experimental medicine and biology·2026
Same journal

Proteomic and Functional Comparison of Extracellular Vesicles from Wild-Type and Lyn-Deficient Stromal Cells.

Advances in experimental medicine and biology·2026
Same journal

Proteomic Analysis of Histone Sequence Variants and Post-translationally Modified Forms.

Advances in experimental medicine and biology·2026
See all related articles

Area of Science:

  • Cardiology
  • Biochemistry
  • Cell Physiology

Background:

  • Myocardial energy transformation is highly efficient, with small free energy differences between ATP supply and demand.
  • Energy deficiency, such as during hypoxia, can critically lower ATP levels, affecting cellular functions.
  • Understanding cardiomyocyte energetics is crucial for addressing cardiac dysfunction.

Purpose of the Study:

  • To investigate the impact of inotropic interventions on myocardial energetics.
  • To evaluate how changes in calcium handling and crossbridge kinetics influence cellular energy consumption.
  • To determine the relationship between contraction economy and cellular energetic status.

Main Methods:

  • Isolated rat cardiomyocytes were used to measure cell shortening, oxygen consumption (VO2), and intracellular calcium transients.

Related Experiment Videos

  • Inotropic interventions included increased extracellular calcium (Ca2+), isoproterenol, and the Ca2+-sensitizing agent EMD 57033.
  • Contraction economy was calculated as the ratio of contraction amplitude to VO2.

    • Main Results:

    • Increased extracellular Ca2+ and isoproterenol significantly reduced contraction economy (contraction amplitude/VO2).
    • The Ca2+-sensitizing agent EMD 57033 did not alter contraction economy.
    • These findings suggest increased costs of ion cycling contribute to reduced energetic efficiency under certain interventions.

    Conclusions:

    • Alterations in ion transport processes, particularly calcium cycling, substantially impact myocardial energetics.
    • Crossbridge kinetics also play a significant role in regulating cellular energy consumption during contraction.
    • These insights are vital for understanding cardiac energy metabolism and developing therapeutic strategies.