In the present work, an elaborate one-dimensional thermofluid model for a human body is presented. By contrast to the existing pure conduction-/perfusion-based models, the proposed methodology couples the arterial fluid dynamics of a human body with a multi-segmental bioheat model of surrounding solid tissues. In the present configuration, arterial flow is included through a network of elastic vessels. More than a dozen solid segments are employed to represent the heat conduction in the surrounding tissues, and each segment is constituted by a multilayered circular cylinder. Such multi-layers allow flexible delineation of the geometry and incorporation of properties of different tissue types. The coupling of solid tissue and fluid models requires subdivision of the arterial circulation into large and small arteries. The heat exchange between tissues and arterial wall occurs by convection in large vessels and by perfusion in small arteries. The core region, including the heart, provides the inlet conditions for the fluid equations. In the proposed model, shivering, sweating, and perfusion changes constitute the basis of the thermoregulatory system. The equations governing flow and heat transfer in the circulatory system are solved using a locally conservative Galerkin approach, and the heat conduction in the surrounding tissues is solved using a standard implicit backward Euler method. To investigate the effectiveness of the proposed model, temperature field evolutions are monitored at different points of the arterial tree and in the surrounding tissue layers. To study the differences due to flow-induced convection effects on thermal balance, the results of the current model are compared against those of the widely used modelling methodologies. The results show that the convection significantly influences the temperature distribution of the solid tissues in the vicinity of the arteries. Thus, the inner convection has a more predominant role in the human body heat balance than previously thought. To demonstrate its capabilities, the proposed new model is used to study different scenarios, including thermoregulation inactivity and variation in surrounding atmospheric conditions.

In this work, heat transfer between fluid flow in elastic tubes and external environment is modeled using a robust finite element approach. The transport of energy is coupled to fluid flow that is linked to the pressure and cross-sectional area variations of the tube. The novel model developed is applied to flow and heat transfer in elastic tubes with different geometric and material properties. The effects of reflections due to discontinuities and bifurcations in the tubes are also investigated. To determine the heat transport by conduction in the elastic walls, a radial heat conduction model is also incorporated. The coupled flow equations are solved using the locally conservative Galerkin finite element method, which provides an explicit element-wise conservation of fluxes. Several simulations are performed for different parametric variations to understand the relevant aspects of heat transfer in flexible elastic tubes. The results show that small temperature fluctuations are possible, inline with the pulsatile flow boundary conditions. It is also observed that increased flexibility of tubes leads to better heat transfer between the fluid and the wall. The results clearly indicate that any flow reflections also increase the heat transfer between the fluid and the wall.

Ageing plays a fundamental role in arterial blood transport and heat transfer within a human body. The aim of this work is to provide a comprehensive methodology, based on biomechanical considerations, for modelling arterial flow and energy exchange mechanisms in the body accounting for age‐induced changes. The study outlines a framework for age‐related modifications within several interlinked subsystems, which include arterial stiffening, heart contractility variations, tissue volume and property changes, and thermoregulatory system deterioration. Some of the proposed age‐dependent governing equations are directly extrapolated from experimental data sets. The computational framework is demonstrated through numerical experiments, which show the impact of such age‐related changes on arterial blood pressure, local temperature distribution, and global body thermal response. The proposed numerical experiments show that the age‐related changes in arterial convection do not significantly affect the tissue temperature distribution. Results also highlight age‐related effects on the sweating mechanism, which lead to a significant reduction in heat dissipation and a subsequent rise in skin and core temperatures.

Arterial wall dynamics arise from the synergy of passive mechano-elastic properties of the vascular tissue and the active contractile behaviour of smooth muscle cells (SMCs) that form the media layer of vessels. We have developed a computational framework that incorporates both these components to account for vascular responses to mechanical and pharmacological stimuli. To validate the proposed framework and demonstrate its potential for testing hypotheses on the pathogenesis of vascular disease, we have employed a number of pharmacological probes that modulate the arterial wall contractile machinery by selectively inhibiting a range of intracellular signalling pathways. Experimental probes used on ring segments from the rabbit central ear artery are: phenylephrine, a selective α1-adrenergic receptor agonist that induces vasoconstriction; cyclopiazonic acid (CPA), a specific inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase; and ryanodine, a diterpenoid that modulates Ca2+ release from the sarcoplasmic reticulum. These interventions were able to delineate the role of membrane versus intracellular signalling, previously identified as main factors in smooth muscle contraction and the generation of vessel tone. Each SMC was modelled by a system of nonlinear differential equations that account for intracellular ionic signalling, and in particular Ca2+ dynamics. Cytosolic Ca2+ concentrations formed the catalytic input to a cross-bridge kinetics model. Contractile output from these cellular components forms the input to the finite-element model of the arterial rings under isometric conditions that reproduces the experimental conditions. The model does not account for the role of the endothelium, as the nitric oxide production was suppressed by the action of L-NAME, and also due to the absence of shear stress on the arterial ring, as the experimental set-up did not involve flow. Simulations generated by the integrated model closely matched experimental observations qualitatively, as well as quantitatively within a range of physiological parametric values. The model also illustrated how increased intercellular coupling led to smooth muscle coordination and the genesis of vascular tone.