ArticleBasic research in cardiology
Mechanical restitution and recirculation fraction in cardiac myocytes and left ventricular muscle of adult rats.
Article in Basic research in cardiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 16 citations in OpenAlex.
- Influence of Amiodarone and Dronedarone on the Force-Interval Dependence of Rat Myocardium.BioMed research international · 2018Article
- Receptor-independent sensitization of the adenylyl cylase after chronic treatment with cyclosporine A.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- Chelerythrine treatment influences the balance of pro- and anti-apoptotic signaling pathways in the remote myocardium after infarction.Molecular and cellular biochemistry · 2008Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unloaded cell shortening was measured in electrically stimulated myocytes from adult rat hearts to compare the contractile response to stimulation with that in isometrically contracting left ventricular papillary muscles under similar experimental conditions, but preloaded to produce maximum twitch tension. Mechanical restitution in cells followed a biexponential function with time constants of 0.19 +/- 0.03 s and 36.4 +/- 10.2 s (7 cells from 5 hearts, n = 7/5). The time constants for papillary muscles were 0.58 +/- 0.05 s and 14.6 +/- 1.0 s (n = 6/6). In myocytes, maximum post-rest potentiation occurred after 30 to 60 s of rest. The potentiation after 60 s of rest was 2.48 +/- 0.31 times the steadystate in cells and 2.63 +/- 0.16 in papillary muscles. Recirculation fraction of C2+ as calculated from the decay of post-rest potentiation was 0.84 +/- 0.04 in single cells and 0.59 +/- 0.02 in papillary muscles (p < 0.005). Caffeine (3mM) abolished post-rest potentiation in both types of preparations. The numerical values for the time constants of mechanical restitution, potentiation factor and recirculation fraction in papillary muscles did not depend on preload. It is concluded that interval-dependent changes of contractility are preserved in single cardiac cells but the kinetics of decay of potentiation appear to have changed quantitatively.
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