ArticleAmerican journal of physiology. Heart and circulatory physiology2015
The Frank-Starling mechanism involves deceleration of cross-bridge kinetics and is preserved in failing human right ventricular myocardium.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Why we need treatment? Prognosis of tricuspid regurgitation.European heart journal supplements : journal of the European Society of Cardiology · 2026Article
- Intrinsic mechanisms of right ventricular autoregulation.Scientific reports · 2024Article
- Cardiovascular Subphenotypes in ARDS: Diagnostic and Therapeutic Implications and Overlap with Other ARDS Subphenotypes.Journal of clinical medicine · 2023Review
- Sarcomere length affects Ca2+ sensitivity of contraction in ischemic but not non-ischemic myocardium.The Journal of general physiology · 2023Article
- The importance of mechanical conditions in the testing of excitation abnormalities in a population of electro-mechanical models of human ventricular cardiomyocytes.Frontiers in physiology · 2023Article
- New mechanistic insights to PLOD1-mediated human vascular disease.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Impact of etiology on force and kinetics of left ventricular end-stage failing human myocardium.Journal of molecular and cellular cardiology · 2021Article
- Mechano-calcium and mechano-electric feedbacks in the human cardiomyocyte analyzed in a mathematical model.The journal of physiological sciences : JPS · 2020Article
- Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium.American journal of physiology. Heart and circulatory physiology · 2019Article
- Extracellular Matrix From Hypertrophic Myocardium Provokes Impaired Twitch Dynamics in Healthy Cardiomyocytes.JACC. Basic to translational science · 2019Article
- Ablation of the calpain-targeted site in cardiac myosin binding protein-C is cardioprotective during ischemia-reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- Regulatory light chain phosphorylation augments length-dependent contraction in PTU-treated rats.The Journal of general physiology · 2019Article
- Length-Dependent Activation of Contractility and Ca-Transient Kinetics in Auxotonically Contracting Isolated Rat Ventricular Cardiomyocytes.Frontiers in physiology · 2019Article
- Myocardial relaxation in human heart failure: Why sarcomere kinetics should be center-stage.Archives of biochemistry and biophysics · 2019Review
- Force-frequency relationship and early relaxation kinetics are preserved upon sarcoplasmic blockade in human myocardium.Physiological reports · 2018Article
- Human Myocardium Has a Robust α1A-Subtype Adrenergic Receptor Inotropic Response.Journal of cardiovascular pharmacology · 2018Article
- Etiology-dependent impairment of relaxation kinetics in right ventricular end-stage failing human myocardium.Journal of molecular and cellular cardiology · 2018Article
- CSI position statement on management of heart failure in India.Indian heart journal · 2018Review
- Defining the molecular signatures of human right heart failure.Life sciences · 2018Article
- Highly variable contractile performance correlates with myocyte content in trabeculae from failing human hearts.Scientific reports · 2018Article
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
Cross-bridge cycling rate is an important determinant of cardiac output, and its alteration can potentially contribute to reduced output in heart failure patients. Additionally, animal studies suggest that this rate can be regulated by muscle length. The purpose of this study was to investigate cross-bridge cycling rate and its regulation by muscle length under near-physiological conditions in intact right ventricular muscles of nonfailing and failing human hearts. We acquired freshly explanted nonfailing (n = 9) and failing (n = 10) human hearts. All experiments were performed on intact right ventricular cardiac trabeculae (n = 40) at physiological temperature and near the normal heart rate range. The failing myocardium showed the typical heart failure phenotype: a negative force-frequency relationship and β-adrenergic desensitization (P < 0.05), indicating the expected pathological myocardium in the right ventricles. We found that there exists a length-dependent regulation of cross-bridge cycling kinetics in human myocardium. Decreasing muscle length accelerated the rate of cross-bridge reattachment (ktr) in both nonfailing and failing myocardium (P < 0.05) equally; there were no major differences between nonfailing and failing myocardium at each respective length (P > 0.05), indicating that this regulatory mechanism is preserved in heart failure. Length-dependent assessment of twitch kinetics mirrored these findings; normalized dF/dt slowed down with increasing length of the muscle and was virtually identical in diseased tissue. This study shows for the first time that muscle length regulates cross-bridge kinetics in human myocardium under near-physiological conditions and that those kinetics are preserved in the right ventricular tissues of heart failure patients.
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