Uppsats

Numerical Modeling of Mouse AorticVasoreactivity - Histo-MechanicalTissue Characterization

Master-uppsats

KTH/Medicinteknik och hälsosystem

Publicerad: 2026

Språk: Engelska

Sammanfattning

Vasoreactivity, i.e. the contraction and dilation of the vessel diameter, is an important active property of blood vessels, mainly driven by Smooth Muscle Cells (SMCs). Through this mechanism, vessels regulate vascular tone and maintain hemodynamic homeostasis. Its study is therefore particularly important, as it can help improve the understanding of vascular pathologies associated with alterations in normal vascular tone, such as hypertension. This thesis, conducted at the Department of Engineering Mechanics (KTH) in Stockholm, aims to investigate mouse aortic vasoreactivity through the implementation of a numerical model. Both passive properties, governed by elastin and collagen, and active properties are analyzed, and the model integrates histological information with experimental pressure–diameter curves obtained from inflation tests of mouse aortas under fully relaxed (passive), maximally contracted (active), and normal tone conditions. The numerical results reproduce, in the fully relaxed (passive) state, the typical s-shaped pressure–diameter curve. An active contribution of SMCs is observed, with a diameter reduction of approximately 19.5% between relaxed and maximally contracted states within the physiological pressure range (10.7 to 16 kPa). Under normal tone conditions, the model predicts an intermediate response, indicating that about 40% of maximal contractile capacity is already engaged basally. The model shows the best agreement with experimental data under normal tone (NRMSE of 7.5%), followed by the active state (12.1%), and the lowest agreement in the passive state (28.4%). Overall, the implemented histo-mechanical model enables a quantitative separation of passive extracellular matrix and active SMC contribution in mouse aortas. This numerical approach can support future studies on vascular tone regulation in cardiovascular disease models.

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