A Multi-Physics Finite Element Model of the Traction Forces in a Three-Dimensional Smooth Muscle Cell

Author(s):  
Marita L. Rodriguez ◽  
Sangyoon J. Han ◽  
Nathan J. Sniadecki

Vascular smooth muscle cells (VSM) modulate cardiac output, maintain vascular pressure, and regulate blood flow via contraction. This contraction is generated by a mechanochemical interaction of actin-myosin cross-bridges within each cell and is governed by the biochemical and mechanical state of the cell [1]. When this state is disturbed, VSM cells can respond with excessive constriction (which can lead to hypertension) or weakened residual stresses (which can result in aortic aneurysms); both of which are considered to be symptoms of cardiovascular diseases [2]. Furthermore, disruption in the state of VSM cells can cause their migration into the intimal layer of the artery, which is a precursor to atherosclerosis.

1989 ◽  
Vol 66 (4) ◽  
pp. 1570-1578 ◽  
Author(s):  
T. S. Hakim ◽  
R. Lisbona ◽  
G. W. Dean

To examine the effect of cardiac output (CO) on the gravity-nondependent distribution of pulmonary blood flow, 2 X 10(6) 99mTc-labeled albumin microspheres (20 microns) were injected at end expiration into dogs (anesthetized, supine, and breathing room air spontaneously). Two animals were injected at their resting CO, two were injected during increased CO (arteriovenous fistulas induced), and two were injected at low CO (phlebotomy induced). The chest was opened and the lungs were removed, drained of blood, and dried while fully inflated. Single-photon emission-computed tomography was performed on the dry lungs to map the distribution of activity in transverse, coronal, and sagittal slices. The results confirmed the presence of a central-peripheral gravity-nondependent gradient and showed that increases in CO were associated with increases in absolute flow to both the central and peripheral regions of the lung with persistence of the central-peripheral gradient. These observations were further confirmed by direct imaging of midcoronal slices. Examination of the average flow in vertical and horizontal slices showed that, when zone 1 was not present, changes in CO affected all slices uniformly, such that when the CO doubled, the absolute flow in every slice in all three planes also doubled. We conclude that, with the exception of recruitment and derecruitment of vascular channels in the upper regions of the lung (zone 1), when CO changes, the blood flow everywhere in the lung changes uniformly and in proportion to the CO. This uniform increase in blood flow is consistent with the three-dimensional nature and resistive properties of the pulmonary vascular tree.


1997 ◽  
Vol 273 (3) ◽  
pp. H1587-H1594 ◽  
Author(s):  
W. J. Vankan ◽  
J. M. Huyghe ◽  
D. W. Slaaf ◽  
C. C. van Donkelaar ◽  
M. R. Drost ◽  
...  

Mechanical interaction between tissue stress and blood perfusion in skeletal muscles plays an important role in blood flow impediment during sustained contraction. The exact mechanism of this interaction is not clear, and experimental investigation of this mechanism is difficult. We developed a finite-element model of the mechanical behavior of blood-perfused muscle tissue, which accounts for mechanical blood-tissue interaction in maximally vasodilated vasculature. Verification of the model was performed by comparing finite-element results of blood pressure and flow with experimental measurements in a muscle that is subject to well-controlled mechanical loading conditions. In addition, we performed simulations of blood perfusion during tetanic, isometric contraction and maximal vasodilation in a simplified, two-dimensional finite-element model of a rat calf muscle. A vascular waterfall in the venous compartment was identified as the main cause for blood flow impediment both in the experiment and in the finite-element simulations. The validated finite-element model offers possibilities for detailed analysis of blood perfusion in three-dimensional muscle models under complicated loading conditions.


2020 ◽  
Vol 27 (7) ◽  
pp. 1081-1088 ◽  
Author(s):  
Eleftherios Spartalis ◽  
Michael Spartalis ◽  
Antonios Athanasiou ◽  
Stavroula A. Paschou ◽  
Nikolaos Patelis ◽  
...  

Inflammation is recognized as a fundamental element in the development and growth of aortic aneurysms. Aortic aneurysm is correlated with aortic wall deformities and injury, as a result of inflammation, matrix metalloproteinases activation, oxidative stress, and apoptosis of vascular smooth muscle cells. The endothelial wall has a critical part in the inflammation of the aorta and endothelial heterogeneity has proven to be significant for modeling aneurysm formation. Endothelial shear stress and blood flow affect the aortic wall through hindrance of cytokines and adhesion molecules excreted by endothelial cells, causing reduction of the inflammation process in the media and adventitia. This pathophysiological process results in the disruption of elastic fibers, degradation of collagen fibers, and destruction of vascular smooth muscle cells. Consequently, the aortic wall is impaired due to reduced thickness, decreased mechanical function, and cannot tolerate the impact of blood flow leading to aortic expansion. Surgery is still considered the mainstay therapy for large aortic aneurysms. The prevention of aortic dilation, though, is based on the hinderance of endothelial dysregulation with drugs, the reduction of reactive oxygen and nitrogen species, and also the reduction of pro-inflammatory molecules and metalloproteinases. Further investigations are required to enlighten the emerging role of endothelial cells in aortic disease.


Author(s):  
Hyun Jin Kim ◽  
C. Alberto Figueroa ◽  
Irene E. Vignon-Clementel ◽  
Kenneth E. Jansen ◽  
Charles A. Taylor

Aortic pressure and flow result from the interaction between the ventricle and the arterial circulation. However, prior three-dimensional simulations of aortic blood flow have either assumed a prescribed velocity profile at the inlet or have computed aortic flow and pressure using an upstream heart model implemented with an explicit approach. In this work, we describe an implicit approach which strongly couples a lumped-parameter heart model with a three-dimensional finite element model of the vascular system. We demonstrate that this approach can be used to compute physiologically-realistic blood flow and pressure waves in three-dimensional arterial models and study the interactions between the heart and the vascular system.


1996 ◽  
Vol 24 (4) ◽  
pp. 339-348 ◽  
Author(s):  
R. M. V. Pidaparti

Abstract A three-dimensional (3D) beam finite element model was developed to investigate the torsional stiffness of a twisted steel-reinforced cord-rubber belt structure. The present 3D beam element takes into account the coupled extension, bending, and twisting deformations characteristic of the complex behavior of cord-rubber composite structures. The extension-twisting coupling due to the twisted nature of the cords was also considered in the finite element model. The results of torsional stiffness obtained from the finite element analysis for twisted cords and the two-ply steel cord-rubber belt structure are compared to the experimental data and other alternate solutions available in the literature. The effects of cord orientation, anisotropy, and rubber core surrounding the twisted cords on the torsional stiffness properties are presented and discussed.


2007 ◽  
Vol 35 (3) ◽  
pp. 226-238 ◽  
Author(s):  
K. M. Jeong ◽  
K. W. Kim ◽  
H. G. Beom ◽  
J. U. Park

Abstract The effects of variations in stiffness and geometry on the nonuniformity of tires are investigated by using the finite element analysis. In order to evaluate tire uniformity, a three-dimensional finite element model of the tire with imperfections is developed. This paper considers how imperfections, such as variations in stiffness or geometry and run-out, contribute to detrimental effects on tire nonuniformity. It is found that the radial force variation of a tire with imperfections depends strongly on the geometrical variations of the tire.


2019 ◽  
Vol 70 (2) ◽  
pp. 718-720
Author(s):  
Lucia Corina Dima-Cozma ◽  
Sebastian Cozma ◽  
Delia Hinganu ◽  
Cristina Mihaela Ghiciuc ◽  
Florin Mitu

Matrix metalloproteinases (MMPs) are the primary mediators of extracellular remodeling and their properties are useful in diagnostic evaluation and treatment. They are zinc-dependent proteases. MMPs have been involved in the mechanisms of atherosclerosis in various arterial areas, ischemic heart disease and myocardial infarction, atrial fibrillation and aortic aneurysms. Recently, MMP9 has been implicated in dyslipidemia and cholesterol synthesis by the liver. Increased MMP expression and activity has been associated with neointimal arterial lesions and migration of smooth muscle cells after arterial balloon dilation, while MMP inhibition decreases smooth muscle cell migration in vivo and in vitro.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Jiang Lan Fan ◽  
Jose A. Rivera ◽  
Wei Sun ◽  
John Peterson ◽  
Henry Haeberle ◽  
...  

AbstractUnderstanding the structure and function of vasculature in the brain requires us to monitor distributed hemodynamics at high spatial and temporal resolution in three-dimensional (3D) volumes in vivo. Currently, a volumetric vasculature imaging method with sub-capillary spatial resolution and blood flow-resolving speed is lacking. Here, using two-photon laser scanning microscopy (TPLSM) with an axially extended Bessel focus, we capture volumetric hemodynamics in the awake mouse brain at a spatiotemporal resolution sufficient for measuring capillary size and blood flow. With Bessel TPLSM, the fluorescence signal of a vessel becomes proportional to its size, which enables convenient intensity-based analysis of vessel dilation and constriction dynamics in large volumes. We observe entrainment of vasodilation and vasoconstriction with pupil diameter and measure 3D blood flow at 99 volumes/second. Demonstrating high-throughput monitoring of hemodynamics in the awake brain, we expect Bessel TPLSM to make broad impacts on neurovasculature research.


1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.


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