Large Human Arteries Research Articles

Dietary Nitrate and Nitric Oxide Metabolism: Mouth, Circulation, Skeletal Muscle, and Exercise Performance.

Nitric oxide (NO) is a gaseous signaling molecule that plays an important role in myriad physiological processes, including the regulation of vascular tone, neurotransmission, mitochondrial respiration, and skeletal muscle contractile function. NO may be produced via the canonical NO synthase-catalyzed oxidation of l-arginine and also by the sequential reduction of nitrate to nitrite and then NO. The body's nitrate stores can be augmented by the ingestion of nitrate-rich foods (primarily green leafy vegetables). NO bioavailability is greatly enhanced by the activity of bacteria residing in the mouth, which reduce nitrate to nitrite, thereby increasing the concentration of circulating nitrite, which can be reduced further to NO in regions of low oxygen availability. Recent investigations have focused on promoting this nitrate-nitrite-NO pathway to positively affect indices of cardiovascular health and exercise tolerance. It has been reported that dietary nitrate supplementation with beetroot juice lowers blood pressure in hypertensive patients, and sodium nitrite supplementation improves vascular endothelial function and reduces the stiffening of large elastic arteries in older humans. Nitrate supplementation has also been shown to enhance skeletal muscle function and to improve exercise performance in some circumstances. Recently, it has been established that nitrate concentration in skeletal muscle is much higher than that in blood and that muscle nitrate stores are exquisitely sensitive to dietary nitrate supplementation and deprivation. In this review, we consider the possibility that nitrate represents an essential storage form of NO and discuss the integrated function of the oral microbiome, circulation, and skeletal muscle in nitrate-nitrite-NO metabolism, as well as the practical relevance for health and performance.

Late-life voluntary wheel running reverses age-related aortic stiffness in mice: a translational model for studying mechanisms of exercise-mediated arterial de-stiffening.

Aortic stiffening, assessed as pulse-wave velocity (PWV), increases with age and is an important antecedent to, and independent predictor of, cardiovascular diseases (CVD) and other clinical disorders of aging. Aerobic exercise promotes lower levels of aortic stiffness in older adults, but the underlying mechanisms are incompletely understood, largely due to inherent challenges of mechanistic studies of large elastic arteries in humans. Voluntary wheel running (VWR) is distinct among experimental animal exercise paradigms in that it allows investigation of the physiologic effects of aerobic training without potential confounding influences of aversive molecular signaling related to forced exercise. In this study, we investigated whether VWR in mice may be a suitable model for mechanistic studies (i.e., "reverse translation") of the beneficial effects of exercise on arterial stiffness in humans. We found that 10weeks of VWR in old mice (~ 28months) reversed age-related elevations in aortic PWV assessed in vivo (Old VWR: 369 ± 19 vs. old sedentary: 439 ± 20cm/s, P < 0.05). The de-stiffening effects of VWR were accompanied by normalization of age-related increases in ex vivo mechanical stiffness of aortic segments and aortic accumulation of collagen-I and advanced glycation end products, as well as lower levels of aortic superoxide and nitrotyrosine. Our results suggest that late-life VWR in mice recapitulates the aortic de-stiffening effects of exercise in humans and indicates important mechanistic roles for decreased oxidative stress and extracellular matrix remodeling. Therefore, VWR is a suitable model for further study of the mechanisms underlying beneficial effects of exercise on arterial stiffness.

MRI and Blood Flow in Human Arteries: Are There Any Adverse Effects?

To explore if there are any adverse effects on blood flow in human beings when they are exposed to high or ultra high intensity magnetic fields in MRI, by investigating both qualitatively and quantitatively the effects of such fields on the velocity of blood and medically significant hemodynamic wall parameters such as wall shear stress (WSS), oscillatory shear index (OSI) and relative residence time (RRT) in four human large arteries. Blood flow in an artery is approximated as a flow through a uniform circular tube with rigid porous walls and the well-known McDonalds model is employed by using pressure gradient waveforms reported in the medical literature. No significant change in the above parameters is observed up to 3T in all these arteries except a discernible change in the velocity and RRT in the pulmonary artery. Very significant changes are noticed in the above parameters beyond 8T in the pulmonary artery. The common hypothesis that low WSS and high OSI co-locate is not acceptable. Our results suggest that the clinical consequences are to be carefully considered before exposing human beings to ultra high field MRI. It may not be appropriate to conclude anything about the effect of magnetic field on blood flow in human beings based on experimental studies on animals, which is one of the reasons for the contradicting reports found in the literature. A slip condition at the wall which is appropriate to hemodynamics is yet to be developed.

Three-Dimensional Full-Field Strain Measurements across a Whole Porcine Aorta Subjected to Tensile Loading Using Optical Coherence Tomography–Digital Volume Correlation

Optical Coherence Tomography (OCT) combined with Digital Volume Correlation (DVC) is a suitable technique to investigate the biomechanical behavior of biological tissues at the microscale. However, to characterize the whole thickness of large human or porcine arteries, the use of osmotic tissue clearing agents, such as propylene glycol, is unavoidable due to intrinsic tissue scattering of light. The mechanical response of biological tissues immersed in tissue clearing agents has been poorly investigated so far. Nevertheless, understanding the mechanisms of tissue clearing could be helpful for developing safe optical-clearing methods for possible in vivo applications. The goal of the present work is to combine OCT and DVC to measure displacement and strain fields in porcine aortic tissues immersed in polypropylene glycol and subjected to stress-relaxation uniaxial tension. Displacement and strain fields are measured across the whole thickness of the porcine aortic wall for the first time. Measurement uncertainties and optimal OCT-DVC parameters are determined to define useful technical recommendations for future similar analyses. It is known that the main effect of polypropylene glycol is a significant increase of collagen fibril packing density due to important loss of water (dehydratation). It results in a pronounced stiffening of the aortic tensile response when compared to the response of the same tissue immersed in PBS. This effect is reversible when the aortic tissue is removed from polypropylene glycol and immersed again in PBS. Another effect is a dramatic reduction of the Poisson’s effect during tensile loading. But the OCT-DVC measured strain fields also reveal heterogeneities of this effect among the different layers of the aorta. It appears that the reduced Poisson’s effect is concentrated in the media layer, whereas the adventitia and intima layer keep a usual Poisson’s effect of nearly incompressible tissues. It is concluded that further work should be conducted on how the smooth muscle cells highly present in the media layer are affected by polypropylene glycol immersion for a better understanding of these effects.

A mathematical modelling on the effect of high intensity magnetic fields on pulsatile blood flow in human arteries

An attempt is made to investigate whether the static magnetic field (SMF) employed in magnetic resonance imaging (MRI) have any adverse effect on the hemodynamic wall parameters in large arteries or not. With the intention of addressing the controversy in the safety issues during MRI exposure, haemodynamics and pathology of large arteries, such as brachial, femoral and pulmonary artery, are compared by varying the intensity of SMF from high to ultrahigh. To be more medically accurate physiological pressure gradient waveforms taken from cardiology literature were digitised and adequate number of harmonics were extracted in order to represent them as Fourier series. All the medically relevant parameters related to endothelial functioning are significantly affected during the time of exposure to ultrahigh intensity SMF, irrespective of the fact whether the artery is closer or away from the heart. In such fields, the fluctuation of Wall Shear Stress (WSS) vector in pulmonary artery is too severe as inferred from oscillatory shear index (OSI) values. The common hypothesis that low WSS and high OSI colocate is not acceptable both in the absence and the presence of magnetic field. It is also inferred that relative residence time can be considered as a single robust metric to predict the pathogenesis of vascular diseases when OSI is moderate. It is felt that more research is necessary, especially to clarify many existing contradictory results in this regard. The controversial reports in the literature of SMF motivated us to mathematically investigate the possible adverse effects of ultrahigh SMFs on pulsatile blood flow in large human arteries and find the maximum intensity of SMF up to which the blood flow and other medically relevant parameters are not significantly affected.

Mathematical investigation of aetiology and pathogenesis of atherosclerosis in human arteries

To understand the role of medically significant hemodynamic wall parameters in the pathogenesis of vascular diseases, pulsatile blood flow in large human arteries of systemic, pulmonary and coronary circulation is investigated by mathematical modelling. To be medically realistic, the pressure gradient waveforms reported in the cardiology literature for the arteries considered are digitised and developed in Fourier series (McDonald's model). Three objectives of the article are to (i) compare qualitatively and quantitatively the pulsatile blood flow between the parallel plate and circular geometry, (ii) compare the hemodynamic wall parameters in the three major circulations mentioned above to gain new medical or physiological insights and (iii) understand if slip at the wall has significant influence on the hemodynamic wall parameters. Our model is reliable since the results obtained here through exact solutions are in great agreement with those reported in the medical literature. New insights gained from our study, documented here for the first time in the hemodynamic literature, are as follows: parallel plate geometry approximation is not reliable quantitatively; larger the radius (Womersley number), larger is the value of relative residence time and hence, higher the probability for vascular diseases; none of the commonly employed interface conditions are suitable for the hemodynamic studies. Comparing our results with earlier studies, we recommend that future research should focus on developing an interface condition exclusively for haemodynamics. We support the recent understanding that low wall shear stress and high oscillatory shear index need not co-locate. We have rendered new physiological insight for this result.

Mathematical investigation of aetiology and pathogenesis of atherosclerosis in human arteries

To understand the role of medically significant hemodynamic wall parameters in the pathogenesis of vascular diseases, pulsatile blood flow in large human arteries of systemic, pulmonary and coronary circulation is investigated by mathematical modelling. To be medically realistic, the pressure gradient waveforms reported in the cardiology literature for the arteries considered are digitised and developed in Fourier series (McDonald's model). Three objectives of the article are to (i) compare qualitatively and quantitatively the pulsatile blood flow between the parallel plate and circular geometry, (ii) compare the hemodynamic wall parameters in the three major circulations mentioned above to gain new medical or physiological insights and (iii) understand if slip at the wall has significant influence on the hemodynamic wall parameters. Our model is reliable since the results obtained here through exact solutions are in great agreement with those reported in the medical literature. New insights gained from our study, documented here for the first time in the hemodynamic literature, are as follows: parallel plate geometry approximation is not reliable quantitatively; larger the radius (Womersley number), larger is the value of relative residence time and hence, higher the probability for vascular diseases; none of the commonly employed interface conditions are suitable for the hemodynamic studies. Comparing our results with earlier studies, we recommend that future research should focus on developing an interface condition exclusively for haemodynamics. We support the recent understanding that low wall shear stress and high oscillatory shear index need not co-locate. We have rendered new physiological insight for this result.

Numerical Investigation of Pulse Wave Propagation in Arteries Using Fluid Structure Interaction Capabilities.

The aim of this study is to present a reliable computational scheme to serve in pulse wave velocity (PWV) assessment in large arteries. Clinicians considered it as an indication of human blood vessels' stiffness. The simulation of PWV was conducted using a 3D elastic tube representing an artery. The constitutive material model specific for vascular applications was applied to the tube material. The fluid was defined with an equation of state representing the blood material. The onset of a velocity pulse was applied at the tube inlet to produce wave propagation. The Coupled Eulerian-Lagrangian (CEL) modeling technique with fluid structure interaction (FSI) was implemented. The scaling of sound speed and its effect on results and computing time is discussed and concluded that a value of 60 m/s was suitable for simulating vascular biomechanical problems. Two methods were used: foot-to-foot measurement of velocity waveforms and slope of the regression line of the wall radial deflection wave peaks throughout a contour plot. Both methods showed coincident results. Results were approximately 6% less than those calculated from the Moens-Korteweg equation. The proposed method was able to describe the increase in the stiffness of the walls of large human arteries via the PWV estimates.

Design and Fabrication of a Conceptual Arterial Ultrasound Phantom Capable of Exhibiting Longitudinal Wall Movement.

The longitudinal movement of the arterial wall of large human arteries has shown promise to be an independent indicator of vascular health. Despite growing interest in this movement, its nature, causes, and implications are not fully understood, and existing phantoms have failed to show a pure longitudinal movement that is not secondary to the distension. An often overlooked aspect of the arterial wall is the interaction between the different layers. The longitudinal movement of the innermost layers, the intima and media, can be several hundred micrometers in the direction of flow during early systole. This is markedly larger than that of the adventitia, indicating that sliding occurs between the two layers. This feature was incorporated into a phantom by casting it in two parts. The molds were developed in-house using mainly a 3-D printer, a versatile and easy production method. Additionally, the phantom contains a tapered region. Using the phantom, we were able to demonstrate a pure longitudinal movement; when it was subjected to a pulsatile pressure, the wall displaced 220 [Formula: see text] (SD 40) radially and 560 [Formula: see text] (SD 74) longitudinally distal to the tapering. The motion followed the pressure variations. This paper serves as a guide for phantom production, explaining each step of the process.

Sinusoïdal flow of blood in a cylindrical deformable vessel exposed to an external magnetic field

The present work provides an analytical solution for the Sinusoidal flow of blood in a cylindrical elastic vessel exposed to an external magnetic field. The vessel is supposed to have non-conducting walls and the induced electric and magnetic fields are neglected. In other words, the well-known calculation of Womersley is revisited through the inclusion of the Lorentz force in the Navier-Stokes equations. A dispersion equation is obtained. This equation admits two types of solutions: the Young waves (mainly associated with radial deformation of the vessel) and the Lamb waves (mainly associated with longitudinal displacements in the vessel wall). It is demonstrated that the external magnetic field has an influence on the wave celerities, on the fluid velocity profiles, and on the wall displacements. It tends to reduce the blood flow and flatten the velocity profile, in the case of Young waves. The pulsatile character of the flow is also dampened. However, these effects become detectable for high values of the Hartmann number ( M > 4, corresponding to B 0 > 36 T with numerical data pertaining to large human arteries) and remain negligible in the context of magnetic resonance imaging ( B 0 ≤ 3 T, or even 7 T).

Numerical Investigation Of Nonlinear Waves Connected To Blood Flow In An Elastic Tube With Variable Radius

Abstract We investigate flow of incompressible fluid in a cylindrical tube with elastic walls. The radius of the tube may change along its length. The discussed problem is connected to the fluid-structure interaction in large human arteries and especially to nonlinear effects. The long-wave approximation is applied to solve model equations. The obtained model Korteweg-deVries equation possessing a variable coefficient is reduced to a nonlinear dynamical system of three first order differential equations. The low probability of a solitary wave arising is shown. Periodic wave solutions of the model system of equations are studied and it is shown that the waves, that are consequence of the irregular heart pulsations may be modelled by a sequence of parts of such periodic wave solutions.

Physiological significance of helical flow in the arterial system and its potential clinical applications.

Helical flow in the human aorta is possibly a typical example of 'form follows function' in the vascular system. The helical blood flow may provide guaranties for the inner surface of the ascending aortic wall to get smooth and even washing by the blood so that atherosclerotic plaques can hardly form in the area of the ascending aorta. It has been documented that the phenomenon of helical flow of blood is not just localized in the ascending aorta, it also exists in several large arteries and veins as well. Preliminary studies demonstrated the widely existing helical flow might play positive physiological roles in facilitating blood flow transport, suppressing disturbed blood flow, preventing the accumulation of atherogenic low density lipoproteins on the luminal surfaces of arteries, enhancing oxygen transport from the blood to the arterial wall and reducing the adhesion of blood cells on the arterial surface. These roles of helical blood flow may lessen the burden of arteries and protect the arteries from the pathology of atherosclerosis, thrombosis, and intimal hyperplasia. The great development of time-resolved three-dimensional phase contrast MRI (flow-sensitive 4D-MRI) and the advent of dimensionless indices such as helical flow index proposed to characterize helical flow make clinic quantification of the helical flow in the human large arteries possible. Moreover, researchers probed into the possibility to apply the mechanism of helical flow to the design of vascular interventions to reduce thrombus formation and intimal hyperplasia caused by abnormal flow conditions.

Cranioselectivity of Sumatriptan Revisited: Pronounced Contractions to Sumatriptan in Small Human Isolated Coronary Artery

Initial concerns about the coronary side-effect potential of the anti-migraine drug sumatriptan and second-generation triptans initiated cranioselectivity studies using proximal human coronary arteries. However, myocardial ischaemia may originate from both large and small human coronary arteries. We investigated the contractions to sumatriptan in proximal (internal diameter 2-3mm), distal (internal diameter 1,000-1,500μm) and small (internal diameter 500-1,000μm) human epicardial coronary arteries and compared these with contractions in the human middle meningeal artery. Concentration response curves to sumatriptan in human coronary arteries were constructed in the absence or presence of the 5-hydroxytryptamine1B (5-HT1B) receptor antagonist SB224289 and the 5-HT1D receptor antagonist BRL15572. The effect of sumatriptan on increased cyclic adenosine monophosphate (cAMP) levels induced by forskolin in proximal and distal coronary artery segments was investigated using a biochemical assay. Western blotting was used to analyse the 5-HT1B receptor density in the human arteries. Contractions in the proximal human coronary artery were significantly smaller than those in the human meningeal artery, as we showed previously. In contrast, contractions to sumatriptan in distal and small human coronary arteries were not different from those in the human meningeal artery. The 5-HT1B receptor antagonist SB224289, but not the 5-HT1D receptor antagonist BRL15572, inhibited the contraction induced by sumatriptan in the coronary arteries. Moreover, in distal, but not in proximal, coronary arteries, sumatriptan inhibited the increase in cAMP levels induced by forskolin. Contrary to our expectations, the 5-HT1B receptor expression was more pronounced in the proximal human coronary artery than in the distal and small human coronary artery. Based on functional experiments in distal and small human coronary arteries, contractions to sumatriptan are not as cranioselective as previously assumed. However, the vast clinical experience with sumatriptan and other triptans has proven that these drugs are cardiovascularly safe when contraindications are taken into account.

Critical Pressure for Arterial Wall Rupture in Major Human Cerebral Arteries

Intracranial bleeding is linked to hemodynamic stress factors, such as hypertension. However, there are no studies that tested the breaking pressure of normal large cerebral arteries in humans. The brains of 10 cadavers (age, 47±14 years; 9 men) were harvested within 48 hours postmortem for 31 segments of the main intracranial arteries. After careful microsurgical preparation, the vessels were pressurized with saline and observed until they ruptured. Vessel diameters averaged 2.6±0.3 mm (range, 1.2-4.3 mm). The average rupture pressure was 2.21±0.59 atm (range, 1.13-4.3 atm) and decreased with age at -0.025 atm/y (R2=40%; P<0.0002). The maximum diameter distention at rupture was 30±9% (13%-52%), which also decreased with age (-0.5%/y; R2=78%; P<0.00001). Neither the rupture pressure nor the maximum distention showed significant dependence on the resting vessel diameter. No significant dependencies were found on the vessel origin, vascular configuration, direction of the rupture, or the presence of minor coexisting pathology. Human cerebral arterial wall breaks only at extremely high intravascular pressures, exceeding several times the highest observed systolic blood pressure, even accounting for age trends. Systolic hypertension alone may not be sufficient to cause intracranial hemorrhage, and there may be additional contributing factors.

Beyond a one‐track mind: understanding blood flow to the brain in humans

Beyond a one‐track mind: understanding blood flow to the brain in humans

The number of cells and the cell proliferation in intima of various human arteries

Increased cell proliferation at the early stages of an atherosclerotic lesion is considered an important stage of development of this pathology, but the degree of the proliferation at various stages of formation of atherosclerotic plaque in various human large arteries so far has been studied insufficiently. In the present work, we studied the thickness of intima and proliferation of the newly “infiltrated” hematogenic and resident cells in atherosclerotic lesion of carotid and coronary arteries; a comparison is also made with similar results obtained on the aorta and presented in our earlier publications. Analysis of thickness of intima and of proliferation in normal intima and at various stages of atherosclerotic lesion (initial stages, lipid strips, lipofibrous plaques, fibrous plaques) showed that, in spite of similar tendencies toward changing the level of infiltration of hematogenic cells and proliferation in various types of arteries, there exist significant quantitative differences between various types of arteries. Thus, it is found that hematogenic cells in lipofibrous plaques of coronary and carotid arteries account for one-third and almost half of the total cell population, respectively, whereas the atherosclerosis-lesioned sites of the aorta, as we showed earlier, contain no more than 15% of hematogenic cells. This allows one to think that the contribution of hemopoietic cells to development of atherosclerosis in carotid and coronary arteries is greater than in the aorta. In spite of differences in the number of the hemopoietic cells accumulating in intima, an analogous bell-shaped dependence of the number of cells on the type of lesion (in the sequence normal intima-initial stages of pathology-lipid strips-lipofibrous plaques-fibrous plaques) was shown for coronary and carotid arteries. Visualization of proliferating (PCNA-positive) cells in atherosclerosed and normal (unchanged) zones of coronary and carotid arteries revealed a similar picture. The maximum number of PCNA-positive resident cells was found in lipofibrous plaques. Changes of the total number of cells were accompanied by a change in the number of proliferating resident and proliferating hematogenic cells.

Numerical simulations of particle dynamics in a poststenotic blood vessel region within the scope of extracorporeal ultrasound stenosis treatment

A numerical model was developed to predict the dynamics of a solid particle in a poststenotic blood vessel region. The flow through a 3D axisymmetric stenosis with 75% reduction in cross-section area was considered for inlet Reynolds numbers of 500 and 1000, which corresponds to typical values for the blood flow in human large arteries. Spherical particles were injected in the flow from the stenosis and tracked using the Discrete Phase Model (DPM) based on a Lagrangian approach. Within the scope of the development of ultrasound thrombolysis methods, the hydrodynamical forces predicted were used to evaluate the residence time of the particle and the minimal ultrasonic intensity required to keep it in the treatment region. For particle sizes larger than 400μm, the intensity required appeared to be compatible with extracorporeal therapeutic ultrasound.

Widespread distribution of HLA-DR-expressing cells in macroscopically undiseased intima of the human aorta: A possible role in surveillance and maintenance of vascular homeostasis

The architectonics and cell composition of the human large arteries are not sufficiently understood. The present study is the first to undertake an analysis of the distribution and quantities of HLA-DR-expressing cells in grossly undiseased human intima using immunohistochemical and immunofluorescent analysis, complemented by the advantages of confocal microscopy. The study revealed a widespread distribution of HLA-DR-expressing cells throughout the intimal space where the cells were integrated into continuous networks via long cell processes. Numbers of HLA-DR+ cells were found to be significantly larger in the middle third of the intima than in the superficial and deep intimal portions. We speculate that a widespread distribution of HLA-DR-expressing cells in the intima of normal human aorta might play a role in the surveillance and maintenance of vascular homeostasis.

The Vasoactive Potential of Kisspeptin-10 in the Peripheral Vasculature

Splice products of the Kiss1 protein (kisspeptins) have been shown to be involved in a diverse range of functions, including puberty, metastasis and vasoconstriction in large human arteries. Circulating Kisspeptin-10 (Kp-10) plasma levels are low in normal individuals but are elevated during various disease states as well as pregnancy. Here, we investigated the potential of Kp-10, the shortest biologically active kisspeptin, to influence microvascular effects, concentrating on the cutaneous vasculature. Kp-10 caused a dose-dependent increase in oedema formation (0.3–10nmol/injection site), assessed by Evans Blue albumin dye extravasation, in the dorsal skin of CD1 mice. Oedema formation was shown to be inhibited by the histamine H1 receptor antagonist mepyramine. The response was characterised by a ring of pallor at the injection site in keeping with vasoconstrictor activity. Therefore, changes in dorsal skin blood flow were assessed by clearance of intradermally injected 99mtechnetium. Kp-10 was found to significantly reduce clearance, in keeping with decreased blood flow and providing further evidence for vasoconstrictor activity. The decreased clearance was partially inhibited by co-treatment with the cyclo-oxygenase inhibitor indomethacin. Finally evidence for the kisspeptin receptor gene (Kiss1R), but not the kisspeptin peptide gene (Kiss1), mRNA expression was observed in heart, aorta and kidney samples from normal and angiotensin II induced hypertensive mice, with similar mRNA levels observed in each. We have evidence for two peripheral vasoactive roles for kisspeptin-10. Firstly, plasma extravasation indicative of ability to induce oedema formation and secondly decreased peripheral blood flow, indicating microvascular constriction. Thus Kp-10 has vasoactive properties in the peripheral microvasculature.

Peculiarities of cell composition and cell proliferation in different type atherosclerotic lesions in carotid and coronary arteries

Increased cell proliferation in early atherosclerotic lesions is recognized as an essential event in atherogenesis but the levels of cell proliferation in the different stages of atherosclerotic plague formation in different types of human large arteries are still insufficiently studied. In the present work, we studied intima thickness and proliferation of newly “infiltrated” hematogenous and resident cells in atherosclerotic lesions of the carotid and coronary arteries and compared these parameters with those in the aorta, which we reported in an earlier publication (Orekhov et al. [8]). Analysis of intima thickness and proliferation in grossly unaffected intima and in different types of atherosclerotic lesions (initial lesions, fatty streaks, lipofibrous plaques, and fibrous plaques) revealed that, although there were similar tendencies in the change of the infiltration levels of hematogenous cells and proliferation in different types of arteries, there were significant quantitative differences between different types of arteries. Hematogenous cells in lipofibrous plaques of the coronary and carotid arteries were found to account for a third and almost for a half of the total cell population, respectively, while atherosclerotic lesions in the aorta, as shown by us previously, contain no more than 15% of hematogenous cells. This suggests that the contribution of hematogenous cells to the development of atherosclerosis in the carotid and coronary arteries appears to be more significant than in the aorta. Despite the differences in the numbers of accumulating hematogenous cells in the intima, a similar “bell-shaped” dependence of cell numbers on the lesion type, involved the following sequence: unaffected intima – initial lesions – fatty streaks – lipofibrous plaques – fibrous plaques, was detected in the coronary and carotid arteries. The visualization of PCNA-positive cells in atherosclerotic and unaffected zones of the coronary and carotid arteries revealed similar patterns of the distribution of proliferating cells. The maximum numbers of PCNA-positive resident cells were identified in lipofibrous plaques. The changes in the total cell numbers were found to be accompanied by the changes in the numbers of both proliferating resident cells and proliferating hematogenous cells. According to our knowledge, this is the first report that provides factual data about the similarities and differences in cell composition and proliferation between different types of large arteries in which the development of atherosclerosis is of crucial importance.