ArticleScientific reports2020
The cardiac work-loop technique: An in vitro model for identifying and profiling drug-induced changes in inotropy using rat papillary muscles.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The importance of muscle activation on the interpretation of muscle mechanical performance.The Journal of experimental biology · 2024Article
- Profiling the Biomechanical Responses to Workload on the Human Myocyte to Explore the Concept of Myocardial Fatigue and Reversibility: Rationale and Design of the POWER Heart Failure Study.Journal of cardiovascular translational research · 2024Article
- Isolated cardiac muscle contracting against a real-time model of systemic and pulmonary cardiovascular loads.American journal of physiology. Heart and circulatory physiology · 2023Article
- Myocardial Fatigue: a Mechano-energetic Concept in Heart Failure.Current cardiology reports · 2022Review
- Mechanisms of flecainide induced negative inotropy: An in silico study.Journal of molecular and cellular cardiology · 2021Article
- Safety pharmacology during the COVID pandemic.Journal of pharmacological and toxicological methodsArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
The cardiac work-loop technique closely mimics the intrinsic in vivo movement and characteristics of cardiac muscle function. In this study, six known inotropes were profiled using the work-loop technique to evaluate the potential of this method to predict inotropy. Papillary muscles from male Sprague-Dawley rats were mounted onto an organ bath perfused with Krebs-Henseleit buffer. Following optimisation, work-loop contractions were performed that included an initial stabilisation period followed by vehicle control or drug administration. Six known inotropes were tested: digoxin, dobutamine, isoprenaline, flecainide, verapamil and atenolol. Muscle performance was evaluated by calculating power output during work-loop contraction. Digoxin, dobutamine and isoprenaline caused a significant increase in power output of muscles when compared to vehicle control. Flecainide, verapamil and atenolol significantly reduced power output of muscles. These changes in power output were reflected in alterations in work loop shapes. This is the first study in which changes in work-loop shape detailing for example the activation, shortening or passive re-lengthening have been linked to the mechanism of action of a compound. This study has demonstrated that the work-loop technique can provide an important novel method with which to assess detailed mechanisms of drug-induced effects on cardiac muscle contractility.
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