Coupling Vibration Analysis of Blood Vessels

2001 ◽  
Author(s):  
Jingliang Miao ◽  
Haixiang Liu
Keyword(s):  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessels ◽  
Dynamic Model ◽  
Natural Frequency ◽  
Vibration Analysis ◽  
Vessel Wall ◽  
Blood Vessel Wall ◽  
Coupled Vibration ◽  
Coupling Vibration

Abstract This paper proposes and analyzes a simple dynamic model of blood vessel wall. By studying the coupled vibration of blood flow and vessel wall, one can get the natural frequency of a blood vessel. The method used here is generalized calculus of variations. The results show that the flexibility of blood vessels has a greater influence on the fundamental frequency of the coupled vibration and the viscosity of blood vessel has little effect on the frequency of the coupled vibration but has a greater effect on the amplitude of the vibration. Therefore it is important to control both the viscosity and flexibility of blood vessels.

scholarly journals INFLUENCE OF AGE AND GENDER ON THE STRENGTH OF BLOOD VESSELS

2016 ◽  
Vol 4 ◽  
pp. 719-726
Author(s):  
Zyta Kuzborska
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Vessel ◽  
Flow Velocity ◽  
Blood Vessels ◽  
Blood Flow Velocity ◽  
Vessel Wall ◽  
Blood Vessel Wall ◽  
Critical Stresses ◽  
And Gender

This article examines the effects of cardiovascular diseases that alter the diameter, wall thickness, and length of blood vessels. Depending on form and size of the damage, blood flow velocity, blood pressure, and stresses are affected in areas of diseased blood vessels. Through stimulating the deviations in the geometric shape of a blood-vessel wall, local blood pressure and stresses can arise from flow variation of blood vessels. This rise affects the blood-vessel wall and causes critical stresses likely to produce fissures in the blood vessels. It was found, that blood vessel pathology could cause blood flow velocity to increase up to 2.2 times and local blood pressure up to 3.4 times, and that human aging may have a significant influence on blood-vessel strength.

Vasculitis

2018 ◽  
Author(s):  
Raashid Luqmani
Keyword(s):  
Connective Tissue ◽  
Blood Vessel ◽  
Blood Vessels ◽  
Vessel Wall ◽  
Connective Tissue Diseases ◽  
Blood Vessel Wall ◽  
Target Organs ◽  
Laboratory Features ◽  
Life Threatening ◽  
Pulmonary Capillaritis

The vasculitides are a heterogeneous group of disorders that can range from mild inflammation of blood vessels in the skin, to organ- and life-threatening diseases. The term ‘vasculitis’ is a pathological description of blood vessel wall inflammation which leads to ischaemia and infarction of the target organs. Definitions and classifications of the primary vasculitides are mainly based on the predominant calibre of the blood vessels involved but incorporate clinical, pathological, and laboratory features. The secondary vasculitides usually occur in the context of other connective tissue diseases and are not discussed further in this section. Goodpasture’s disease is not usually included in the primary vasculitides, but has compatible clinical features of pulmonary capillaritis and glomerulonephritis.

Effects of Cyclic Motion on Coronary Blood Flow

2013 ◽  
Vol 135 (12) ◽  
Author(s):  
Mahmudul Hasan ◽  
David A. Rubenstein ◽  
Wei Yin
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Blood Vessel ◽  
Coronary Blood Flow ◽  
Vessel Wall ◽  
Wall Stress ◽  
Blood Vessel Wall ◽  
Flow Parameters ◽  
Cyclic Motion

The goal of this study was to establish a computational fluid dynamics model to investigate the effect of cyclic motion (i.e., bending and stretching) on coronary blood flow. The three-dimensional (3D) geometry of a 50-mm section of the left anterior descending artery (normal or with a 60% stenosis) was constructed based on anatomical studies. To describe the bending motion of the blood vessel wall, arbitrary Lagrangian–Eularian methods were used. To simulate artery bending and blood pressure change induced stretching, the arterial wall was modeled as an anisotropic nonlinear elastic solid using the five-parameter Mooney–Rivlin hyperelastic model. Employing a laminar model, the flow field was solved using the continuity equations and Navier–Stokes equations. Blood was modeled as an incompressible Newtonian fluid. A fluid–structure interaction approach was used to couple the fluid domain and the solid domain iteratively, allowing force and total mesh displacement to be transferred between the two domains. The results demonstrated that even though the bending motion of the coronary artery could significantly affect blood cell trajectory, it had little effect on flow parameters, i.e., blood flow velocity, blood shear stress, and wall shear stress. The shape of the stenosis (asymmetric or symmetric) hardly affected flow parameters either. However, wall normal stresses (axial, circumferential, and radial stress) can be greatly affected by the blood vessel wall motion. The axial wall stress was significantly higher than the circumferential and radial stresses, as well as wall shear stress. Therefore, investigation on effects of wall stress on blood vessel wall cellular functions may help us better understand the mechanism of mechanical stress induced cardiovascular disease.

Influence of Tensile Strain on Smooth Muscle Cell Orientation in Rat Blood Vessels

1998 ◽  
Vol 120 (3) ◽  
pp. 313-320 ◽  
Author(s):  
S. Q. Liu
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Blood Vessels ◽  
Vessel Wall ◽  
Tensile Strain ◽  
Longitudinal Direction ◽  
Blood Vessel Wall ◽  
Vein Grafts ◽  
Observation Times ◽  
Strain Direction

Blood vessels are subject to tensile stress and associated strain which may influence the structure and organization of smooth muscle cells (SMCs) during physiological development and pathological remodeling. This study focused on the influence of the major tensile strain on the SMC orientation in the blood vessel wall. Several blood vessels, including the aorta, the mesenteric artery and vein, and the jugular vein of the rat were used to observe the normal distribution of tensile strains and SMC orientation; and a vein graft model was used to observe the influence of altered strain direction on the SMC orientation. The circumferential and longitudinal strains in these blood vessels were measured by using a biomechanical technique, and the SMC orientation was examined by fluorescent microscopy at times of 10, 20, and 30 days. Results showed that the SMCs were mainly oriented in the circumferential direction of straight blood vessels with an average angle of ~85 deg between the SMC axis and the vessel axis in all observed cases. The SMC orientation coincided with the principal direction of the circumferential strain, a major tensile strain, in the blood vessel wall. In vein grafts, the major tensile strain direction changed from the circumferential to the longitudinal direction at observation times of 10, 20, and 30 days after graft surgery. This change was associated with a decrease in the angle between the axis of newly proliferated SMCs and that of the vessel at all observation times (43 ± 11 deg, 42 ± 10 deg, and 41 ± 10 deg for days 10, 20, and 30, respectively), indicating a shift of the SMC orientation from the circumferential toward the longitudinal direction. These results suggested that the major tensile strain might play a role in the regulation of SMC orientation during the development of normal blood vessels as well as during remodeling of vein grafts.

scholarly journals How leukocytes trigger opening and sealing of gaps in the endothelial barrier

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2321 ◽  
Author(s):  
Debashree Goswami ◽  
Dietmar Vestweber
Keyword(s):  
Endothelial Cells ◽  
Blood Vessel ◽  
Blood Vessels ◽  
Immune Cells ◽  
Molecular Basis ◽  
Vessel Wall ◽  
Endothelial Barrier ◽  
Apical Surface ◽  
Blood Vessel Wall ◽  
Inner Surface

The entry of leukocytes into tissues requires well-coordinated interactions between the immune cells and endothelial cells which form the inner lining of blood vessels. The molecular basis for recognition, capture, and adhesion of leukocytes to the endothelial apical surface is well studied. This review will focus on recent advances in our understanding of events following the firm interaction of leukocytes with the inner surface of the blood vessel wall. We will discuss how leukocytes initiate the transmigration (diapedesis) process, trigger the opening of gaps in the endothelial barrier, and eventually move through this boundary.

The Intravascular Generation of Fibrinogen Derivatives and the Blood Vessel Wall in Venous Thrombosis and Disseminated Intravascular Coagulation

1977 ◽  
Vol 38 (04) ◽  
pp. 0831-0849 ◽  
Author(s):  
Gwendolyn J. Stewart
Keyword(s):  
Blood Vessel ◽  
Venous Thrombosis ◽  
Vessel Wall ◽  
Fluid Phase ◽  
Primary Site ◽  
Blood Vessel Wall ◽  
Fibrin Deposition ◽  
Tissue Destruction ◽  
Fibrin Formation ◽  
Rich Material

SummaryBoth deep venous thrombosis and DIC are intermediate mechanisms of disease – both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.

COMPARISON OF ANTIHYPERTENSIVE EFFECT OF MOXONIDINE VERSUS CLONIDINE IN RENAL FAILURE PATIENTS.

2018 ◽  
Vol 6 (9) ◽  
Author(s):  
DR.MATHEW GEORGE ◽  
DR.LINCY JOSEPH ◽  
MRS.DEEPTHI MATHEW ◽  
ALISHA MARIA SHAJI ◽  
BIJI JOSEPH ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Antihypertensive Effect ◽  
The Body ◽  
Ability To Work ◽  
Blood Flows

Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged(1). High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.

scholarly journals Eicosanoids and the blood vessel wall.

Circulation ◽  
1984 ◽  
Vol 70 (4) ◽  
pp. 523-528 ◽  
Author(s):  
P J Cannon
Keyword(s):  
Blood Vessel ◽  
Vessel Wall ◽  
Blood Vessel Wall
Sign in / Sign up

Export Citation Format

Share Document