Vessel Wall Compliance and Transient Fluid Movement

1989 ◽  
pp. 203-217
Author(s):  
Perry L. Blackshear ◽  
Gertrude L. Blackshear ◽  
Paul F. Emerson
Keyword(s):  
Vessel Wall ◽  
Fluid Movement ◽  
Wall Compliance

Regular endurance exercise in young men increases arterial baroreflex sensitivity through neural alteration of baroreflex arc

2009 ◽  
Vol 106 (5) ◽  
pp. 1499-1505 ◽  
Author(s):  
Hidehiko Komine ◽  
Jun Sugawara ◽  
Koichiro Hayashi ◽  
Mutsuko Yoshizawa ◽  
Takashi Yokoi
Keyword(s):  
Carotid Artery ◽  
Endurance Exercise ◽  
Vessel Wall ◽  
Baroreflex Sensitivity ◽  
Arterial Compliance ◽  
Young Men ◽  
Arterial Baroreflex ◽  
Wall Compliance ◽  
Carotid Arterial ◽  
Arterial Baroreflex Sensitivity

Endurance exercise training increases arterial baroreflex sensitivity that corresponds to alteration in vessel wall compliance of the carotid artery in elderly men. Here, we examined whether regular endurance exercise increases arterial baroreflex sensitivity through neural alteration of the baroreflex arc in young men. We assessed arterial baroreflex sensitivity in eight sedentary men (age 24 ± 1 yr) and nine men trained in endurance exercise (age 23 ± 1 yr) during phase IV of the Valsalva maneuver [systolic arterial blood pressure (SAP)–R-R interval relationship]. Arterial baroreflex sensitivity was further analyzed by dividing the mechanical component [SAP–end-systolic carotid lumen diameter relationship (ultrasonography)] and the neural component (end-systolic carotid lumen diameter–R-R interval relationship). Carotid arterial compliance was determined using B-mode ultrasound and arterial applanation tonometry on the common carotid artery. Arterial baroreflex sensitivity and its neural component were greater in the exercise-trained group ( P < 0.05). In contrast, carotid arterial compliance and the mechanical component of arterial baroreflex sensitivity did not differ between groups. These results suggest that regular endurance exercise in young men increases arterial baroreflex sensitivity through changes in the neural component of the baroreflex arc and not through alterations in vessel wall compliance of the carotid artery.

scholarly journals Effect of Wall Compliance and Permeability on Blood-Flow Rate in Counter-Current Microvessels Formed From Anastomosis During Tumor-Induced Angiogenesis

2012 ◽  
Vol 134 (4) ◽  
Author(s):  
Peng Guo ◽  
Bingmei M. Fu
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Vessel Wall ◽  
Interstitial Fluid ◽  
Tumor Tissue ◽  
Blood Flow Rate ◽  
Tumor Vasculature ◽  
Negligible Effect ◽  
Wall Compliance ◽  
Counter Current

Tumor blood-flow is inhomogeneous because of heterogeneity in tumor vasculature, vessel-wall leakiness, and compliance. Experimental studies have shown that normalization of tumor vasculature by antiangiogenic therapy can improve tumor microcirculation and enhance the delivery of therapeutic agents to tumors. To elucidate the quantitative relationship between the vessel-wall compliance and permeability and the blood-flow rate in the microvessels of the tumor tissue, the tumor tissue with the normalized vasculature, and the normal tissue, we developed a transport model to simultaneously predict the interstitial fluid pressure (IFP), interstitial fluid velocity (IFV) and the blood-flow rate in a counter-current microvessel loop, which occurs from anastomosis in tumor-induced angiogenesis during tumor growth. Our model predicts that although the vessel-wall leakiness greatly affects the IFP and IFV, it has a negligible effect on the intravascular driving force (pressure gradient) for both rigid and compliant vessels, and thus a negligible effect on the blood-flow rate if the vessel wall is rigid. In contrast, the wall compliance contributes moderately to the IFP and IFV, but significantly to the vessel radius and to the blood-flow rate. However, the combined effects of vessel leakiness and compliance can increase IFP, which leads to a partial collapse in the blood vessels and an increase in the flow resistance. Furthermore, our model predictions speculate a new approach for enhancing drug delivery to tumor by modulating the vessel-wall compliance in addition to reducing the vessel-wall leakiness and normalizing the vessel density.

scholarly journals Role of Arterial Pressure, Wall Stiffness, Pulse Pressure and Waveform in Arterial Wall Stress/Strain and Its Clinical Implications

2021 ◽  
Author(s):  
Thomas K. Day
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Vessel Wall ◽  
Arterial Wall ◽  
Clinical Implications ◽  
Pulse Waveform ◽  
Wall Stiffness ◽  
Wall Compliance ◽  
Formaldehyde Vapour

Biomechanical stress applied to the intima of arteries has long been suspected as a factor in the initiation and localisation of atherosclerotic plaque, and it is implicated in the separation of plaque from the underlying arterial wall giving rise to the acute clinical consequences of thrombosis, dissection and embolism. The factors underlying transmural stress were investigated in-vitro using fresh porcine abdominal aortas on an experimental rig in which pulse pressure, pulse waveform, fluid viscosity, pulse rate, vessel wall compliance and systolic and diastolic blood pressure could be varied at will. Vessel wall compliance was progressively reduced by exposure of the artery to formaldehyde vapour for increased periods of time, a saline-treated artery being used as control. Centripetal transmural stress (CTS) and strain were studied by direct observation of the displacement of a compliant false intima (FI) using real-time B and M mode ultrasound, and by measuring the differential pressure between the space beneath the FI and the adjacent vessel lumen. CTS was found to be directly related to pulse pressure (r = 0.907, p < 0.001) and inversely related to vessel wall compliance. It was independently affected by ranked peak pressure waveform (R = 0.93, p < 0.01) being higher with sharp peak pressure and lower when the waveform was rounded, and it peaked in early diastole in untreated vessels, and both in diastole and peak systole in ones stiffened by formaldehyde vapour. Mean arterial pressure exerted a profound effect via its effect on vessel wall stiffness, which was found to rise 7-fold across the mean arterial pressure range 50-130 mmHg and continued to increase in a logarithmic fashion as the upper physiological range of mean arterial pressure was exceeded. There are two potential clinical implications: in mitigating the postulated biomechanical aspects atherogenesis and atherosclerotic plaque detachment, maintaining large vessel wall compliance is important, and the main factor determining this in a healthy artery is mean arterial pressure; if the arterial wall has already become stiffened as a result of disease, and in the absence of critical stenosis, the findings suggest that the appropriate therapeutic targets are modification of pulse pressure and pulse waveform profile. Simply reducing the diastolic pressure in elderly patients may be unwise if the result is a widened pulse pressure and increased transmural strain. The distribution of atheroma at points of focal mechanical strain in the vessel wall may be explicable if the stress induced by an excessive pulse pressure provokes the inflammatory changes seen in repetitive strain injury. Investigation of inflammatory signalling in the vessel wall provoked by repeated mechanical stress may represent a productive area for future research.

scholarly journals The Effect of Poststenotic Vessel Wall Compliance upon the Pulsus Tardus Phenomenon

Angiology ◽  
1994 ◽  
Vol 45 (7) ◽  
pp. 605-611 ◽  
Author(s):  
Ronald O. Bude ◽  
Jonathan M. Rubin ◽  
Joel F. Platt ◽  
Ronald S. Adler
Keyword(s):  
Vessel Wall ◽  
Wall Compliance

The molecular mechanism of mechanotransduction in vascular homeostasis and disease

2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa
Keyword(s):  
Shear Stress ◽  
Blood Vessels ◽  
Vessel Wall ◽  
Vascular Diseases ◽  
Cell Interactions ◽  
Aortic Aneurysms ◽  
Cyclic Stretch ◽  
Mechanical Stimuli ◽  
Vascular Homeostasis ◽  
Matrix Cell

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.

Oxidative Stress and Atherosclerosis: Its Relationship to Growth Factors, Thrombus Formation and Therapeutic Approaches

1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factors ◽  
Vessel Wall ◽  
Inflammatory Responses ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
Vascular Lesion ◽  
Coagulation System ◽  
Therapeutic Approaches ◽  
Causative Relationship

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.

Mechanisms Involved in Platelet Vessel Wall Interaction

1995 ◽  
Vol 74 (01) ◽  
pp. 369-372 ◽  
Author(s):  
Jacek Hawiger
Keyword(s):  
Vessel Wall ◽  
Wall Interaction
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