Key result
Arterial energy dissipation stabilizes pulsatile flow and modulates ventricular-arterial coupling via mechanobiological regulation.
Why the study?
Arterial mechanical behaviour is commonly described using predominantly elastic models that overlook the thermodynamic significance of viscous energy loss, leaving uncertain whether arterial energy dissipation represents a passive loss or a consequence of physiological regulatory processes.
Answers are grounded in this paper and cite their sources.
This paper proposes a thermodynamic framework interpreting arterial energy dissipation not as a passive loss, but as an emergent consequence of multi-scale mechanobiological regulation of arterial mechanical state and vascular impedance.
The mechanical behaviour of arteries is commonly described using predominantly elastic models that overlook the thermodynamic significance of viscous energy loss. Here, we examine whether arterial energy dissipation should be interpreted as a passive loss or as a consequence of physiological processes that regulate arterial function. Building on an intellectual lineage extending from Leonardo da Vinci to modern non-equilibrium thermodynamics, we integrate evidence from in vivo pressure–diameter hysteresis measurements, vascular smooth muscle energetics, endothelial signalling and systemic pressure–volume loop analysis. Together, these observations indicate that arterial dissipation is closely linked to the dynamic regulation of arterial mechanical state, including arterial diameter, stiffness, viscoelasticity, pulse wave velocity and vascular impedance. Experimental and modelling evidence further suggests that viscous energy loss contributes to the stabilization of pulsatile flow and the modulation of ventricular–arterial coupling, while providing a unified thermodynamic interpretation of vascular ageing, hypertension, exercise-induced adaptation and arterial mechanical remodelling. We propose that arterial energy dissipation is best understood not as a directly regulated variable, but as a thermodynamic consequence of the distributed mechanobiological regulation of arterial mechanical state and vascular impedance throughout the arterial network. This framework opens the possibility of defining vascular energetic phenotypes that capture how differences in arterial mechanical regulation shape cardiovascular function and adaptation.
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Armentano et al. (2026) conducted a review in Arterial mechanical function, vascular ageing, and hypertension. Arterial energy dissipation vs. Predominantly elastic models was evaluated. Arterial energy dissipation is an emergent thermodynamic consequence of multi-scale mechanobiological regulation that stabilizes pulsatile flow and modulates ventricular-arterial coupling.
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