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Article

Friction in Myocardial Anoxia Leads to Negative Excess Entropy Production, Self-Organization, and Dissipative Structures

1
Centre de Recherche Clinique, Grand Hôpital de l’Est Francilien, 77100 Meaux, France
2
Department of Pharmaceutical Sciences, University of Antwerp, 2180 Wilrijk, Belgium
3
Institut de Cardiologie, Hôpital de la Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, 75013 Paris, France
4
Département de Chirurgie Thoracique, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Paris-Descartes Université, Assistance Publique-Hôpitaux de Paris, 75014 Paris, France
5
Department of Epidemiology-Data-Biostatistics, Delegation of Clinical Research and Innovation, Foch Hospital, 92150 Suresnes, France
*
Author to whom correspondence should be addressed.
Academic Editors: José S. Urieta, Federico Fogolari and Ana M. Mainar
Int. J. Mol. Sci. 2022, 23(13), 6967; https://doi.org/10.3390/ijms23136967
Received: 16 April 2022 / Revised: 11 June 2022 / Accepted: 21 June 2022 / Published: 23 June 2022
Contraction of the heart is caused by actin filaments sliding along myosin filaments. This generates a frictional force inducing wear of the contractile apparatus. We postulated that this process could be exacerbated when the heart was submitted to severe anoxia. Anoxia induced dramatic abnormalities in the molecular properties of actin-myosin crossbridges. We applied the formalism of far-from-equilibrium thermodynamics to the left ventricular papillary muscles (LVPMs) of mammalian rat hearts which had been subjected to a prolonged anoxia (3 h). We showed that when subjected to prolonged anoxia, the heart operated far-from-equilibrium as evidenced by the non-linearity between thermodynamic force (F/T: Frictional force/Kelvin temperature) and thermodynamic flow (v0: myofilament sliding velocity). The rate of entropy production (EPR) was the product of (F/T) and v0. The excess entropy production (EEP) was equal to δ2St = FTδvo; (S: entropy). The tribological system remained stable when EEP was positive and became unstable when EEP became negative, thus characterizing instability of the system and reflecting the occurrence of self-organization and possibly dissipative structures. After 3 h anoxia, re-oxygenation induced significant reversibility. About 20% of the myosin heads did not recover despite re-oxygenation. These results may be of importance in the context of heart transplantation where the delay between the time of sampling from the donor and the time of the graft installation in the recipient should be as short as possible. View Full-Text
Keywords: friction; myocardium; anoxia; far-from-equilibrium thermodynamics; excess entropy production; self-organisation; dissipative structures friction; myocardium; anoxia; far-from-equilibrium thermodynamics; excess entropy production; self-organisation; dissipative structures
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MDPI and ACS Style

Lecarpentier, Y.; Claes, V.; Hébert, J.-L.; Krokidis, X.; Schussler, O.; Vallée, A. Friction in Myocardial Anoxia Leads to Negative Excess Entropy Production, Self-Organization, and Dissipative Structures. Int. J. Mol. Sci. 2022, 23, 6967. https://doi.org/10.3390/ijms23136967

AMA Style

Lecarpentier Y, Claes V, Hébert J-L, Krokidis X, Schussler O, Vallée A. Friction in Myocardial Anoxia Leads to Negative Excess Entropy Production, Self-Organization, and Dissipative Structures. International Journal of Molecular Sciences. 2022; 23(13):6967. https://doi.org/10.3390/ijms23136967

Chicago/Turabian Style

Lecarpentier, Yves, Victor Claes, Jean-Louis Hébert, Xénophon Krokidis, Olivier Schussler, and Alexandre Vallée. 2022. "Friction in Myocardial Anoxia Leads to Negative Excess Entropy Production, Self-Organization, and Dissipative Structures" International Journal of Molecular Sciences 23, no. 13: 6967. https://doi.org/10.3390/ijms23136967

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