Peripheral arterial volume distensibility changes with applied external pressure: significant difference between arteries with different compliance

This study aimed to quantify the different effect of external cuff pressure on arterial volume distensibility between peripheral arteries with different compliance. 30 healthy subjects were studied with the arm at two positions (0° and 45° from the horizontal level) to introduce different compliance of arteries. The electrocardiogram and finger and ear photoplethysmograms were recorded simultaneously under five external cuff pressures (0, 10, 20, 30 and 40 mmHg) on the whole arm to obtain arterial volume distensibility. With the applied external cuff pressures of 10, 20, 30 and 40 mmHg, the overall changes in arterial volume distensibility referred to those without external pressure were 0.010, 0.029, 0.054 and 0.108% per mmHg for the arm at the horizontal level, and 0.026, 0.071, 0.170 and 0.389% per mmHg for the arm at 45° from the horizontal level, confirming the non-linearity between arterial volume distensibility and external pressure. More interestingly, the significant differences in arterial volume distensibility changes were observed between the two arm positions, which were 0.016, 0.043, 0.116 and 0.281% per mmHg (all P < 0.01). Our findings demonstrated that arterial volume distensibility of peripheral arm arteries increased with external pressure, with a greater effect for more compliant arteries

Tissue Doppler imaging of carotid plaque wall motion: a pilot study

BACKGROUND: Studies suggest the physical and mechanical properties of vessel walls and plaque may be of clinical value in the diagnosis and treatment of cardiovascular atherosclerotic disease. The purpose of this pilot study was to investigate the potential clinical application of ultrasound Tissue Doppler Imaging (TDI) of Arterial Wall Motion (AWM) and to quantify simple wall motion indices in normal and diseased carotid arteries. METHODS: 224 normal and diseased carotid arteries (0–100% stenoses) were imaged in 126 patients (age 25–88 years, mean 68 ± 11). Longitudinal sections of the carotid bifurcation were imaged using a Philips HDI5000 scanner and L12-5 probe under optimized TDI settings. Temporal and spatial AWMs were analyzed to evaluate the vessel wall displacements and spatial gradients at peak systole averaged over 5 cardiac cycles. RESULTS: AWM data were successfully extracted in 91% of cases. Within the carotid bifurcation/plaque region, the maximum wall dilation at peak systole ranged from -100 to 750 microns, mean 335 ± 138 microns. Maximum wall dilation spatial gradients ranged 0–0.49, mean 0.14 ± 0.08. The AWM parameters showed a wide variation and had poor correlation with stenoses severity. Case studies illustrated a variety of pertinent qualitative and quantitative wall motion features related to the biophysics of arterial disease. CONCLUSION: Our clinical experience, using a challenging but realistic imaging protocol, suggests the use of simple quantitative AWM measures may have limitations due to high variability. Despite this, pertinent features of AWM in normal and diseased arteries demonstrate the potential clinical benefit of the biomechanical information provided by TDI

Wall shear stress as measured in vivo: consequences for the design of the arterial system

Based upon theory, wall shear stress (WSS), an important determinant of endothelial function and gene expression, has been assumed to be constant along the arterial tree and the same in a particular artery across species. In vivo measurements of WSS, however, have shown that these assumptions are far from valid. In this survey we will discuss the assessment of WSS in the arterial system in vivo and present the results obtained in large arteries and arterioles. In vivo WSS can be estimated from wall shear rate, as derived from non-invasively recorded velocity profiles, and whole blood viscosity in large arteries and plasma viscosity in arterioles, avoiding theoretical assumptions. In large arteries velocity profiles can be recorded by means of a specially designed ultrasound system and in arterioles via optical techniques using fluorescent flow velocity tracers. It is shown that in humans mean WSS is substantially higher in the carotid artery (1.1–1.3 Pa) than in the brachial (0.4–0.5 Pa) and femoral (0.3–0.5 Pa) arteries. Also in animals mean WSS varies substantially along the arterial tree. Mean WSS in arterioles varies between about 1.0 and 5.0 Pa in the various studies and is dependent on the site of measurement in these vessels. Across species mean WSS in a particular artery decreases linearly with body mass, e.g., in the infra-renal aorta from 8.8 Pa in mice to 0.5 Pa in humans. The observation that mean WSS is far from constant along the arterial tree implies that Murray’s cube law on flow-diameter relations cannot be applied to the whole arterial system. Because blood flow velocity is not constant along the arterial tree either, a square law also does not hold. The exponent in the power law likely varies along the arterial system, probably from 2 in large arteries near the heart to 3 in arterioles. The in vivo findings also imply that in in vitro studies no average shear stress value can be taken to study effects on endothelial cells derived from different vascular areas or from the same artery in different species. The cells have to be studied under the shear stress conditions they are exposed to in real life

Does the principle of minimum work apply at the carotid bifurcation: a retrospective cohort study

<p>Abstract</p> <p>Background</p> <p>There is recent interest in the role of carotid bifurcation anatomy, geometry and hemodynamic factors in the pathogenesis of carotid artery atherosclerosis. Certain anatomical and geometric configurations at the carotid bifurcation have been linked to disturbed flow. It has been proposed that vascular dimensions are selected to minimize energy required to maintain blood flow, and that this occurs when an exponent of 3 relates the radii of parent and daughter arteries. We evaluate whether the dimensions of bifurcation of the extracranial carotid artery follow this principle of minimum work.</p> <p>Methods</p> <p>This study involved subjects who had computed tomographic angiography (CTA) at our institution between 2006 and 2007. Radii of the common, internal and external carotid arteries were determined. The exponent was determined for individual bifurcations using numerical methods and for the sample using nonlinear regression.</p> <p>Results</p> <p>Mean age for 45 participants was 56.9 ± 16.5 years with 26 males. Prevalence of vascular risk factors was: hypertension-48%, smoking-23%, diabetes-16.7%, hyperlipidemia-51%, ischemic heart disease-18.7%.</p> <p>The value of the exponent ranged from 1.3 to 1.6, depending on estimation methodology.</p> <p>Conclusions</p> <p>The principle of minimum work (defined by an exponent of 3) may not apply at the carotid bifurcation. Additional factors may play a role in the relationship between the radii of the parent and daughter vessels.</p

Extension of Murray's law using a non-Newtonian model of blood flow

<p>Abstract</p> <p>Background</p> <p>So far, none of the existing methods on Murray's law deal with the non-Newtonian behavior of blood flow although the non-Newtonian approach for blood flow modelling looks more accurate.</p> <p>Modeling</p> <p>In the present paper, Murray's law which is applicable to an arterial bifurcation, is generalized to a non-Newtonian blood flow model (power-law model). When the vessel size reaches the capillary limitation, blood can be modeled using a non-Newtonian constitutive equation. It is assumed two different constraints in addition to the pumping power: the volume constraint or the surface constraint (related to the internal surface of the vessel). For a seek of generality, the relationships are given for an arbitrary number of daughter vessels. It is shown that for a cost function including the volume constraint, classical Murray's law remains valid (i.e. Σ<it>R</it>^{<it>c </it>}= <it>cste </it>with <it>c </it>= 3 is verified and is independent of <it>n</it>, the dimensionless index in the viscosity equation; <it>R </it>being the radius of the vessel). On the contrary, for a cost function including the surface constraint, different values of <it>c </it>may be calculated depending on the value of <it>n</it>.</p> <p>Results</p> <p>We find that <it>c </it>varies for blood from 2.42 to 3 depending on the constraint and the fluid properties. For the Newtonian model, the surface constraint leads to <it>c </it>= 2.5. The cost function (based on the surface constraint) can be related to entropy generation, by dividing it by the temperature.</p> <p>Conclusion</p> <p>It is demonstrated that the entropy generated in all the daughter vessels is greater than the entropy generated in the parent vessel. Furthermore, it is shown that the difference of entropy generation between the parent and daughter vessels is smaller for a non-Newtonian fluid than for a Newtonian fluid.</p

Microstructural analysis of deformation-induced hypoxic damage in skeletal muscle

Deep pressure ulcers are caused by sustained mechanical loading and involve skeletal muscle tissue injury. The exact underlying mechanisms are unclear, and the prevalence is high. Our hypothesis is that the aetiology is dominated by cellular deformation (Bouten et al. in Ann Biomed Eng 29:153–63, 2001; Breuls et al. in Ann Biomed Eng 31:1357–364, 2003; Stekelenburg et al. in J App Physiol 100(6):1946–954, 2006) and deformation-induced ischaemia. The experimental observation that mechanical compression induced a pattern of interspersed healthy and dead cells in skeletal muscle (Stekelenburg et al. in J App Physiol 100(6):1946–954, 2006) strongly suggests to take into account the muscle microstructure in studying damage development. The present paper describes a computational model for deformation-induced hypoxic damage in skeletal muscle tissue. Dead cells stop consuming oxygen and are assumed to decrease in stiffness due to loss of structure. The questions addressed are if these two consequences of cell death influence the development of cell injury in the remaining cells. The results show that weakening of dead cells indeed affects the damage accumulation in other cells. Further, the fact that cells stop consuming oxygen after they have died, delays cell death of other cells