Arterial Wall Tissue Research Articles

Chapter 10 Human Arterial Wall Cells and Tissues in Culture

This chapter describes the human arterial wall cells and tissues in culture. Human arterial wall explants and isolated smooth muscle cells (SMCs) have been examined by methods of cell culture for several purposes such as morphological phenotypic stability and replicative characteristics and replicative life span. Arterial wall SMCs derived from the media have been cultivated from tissues obtained at surgery or postmortem. Tissue fragments 1–2 mm in diameter are generally used in this procedure. To obtain these fragments, tissue is aseptically removed from the desired organ and placed on a sterile petri plate. The tissue is minced into smaller and smaller pieces with the use of scalpel blades until the desired size is obtained. Human SMCs grow in the same types of media and at the same serum concentrations that have been used successfully for human and animal fibroblasts. SMCs from human fetal aortas undergo senescent changes and cease dividing after 20 passage generations.

Enhanced oxygen uptake and lactate production of smooth muscle cell proliferates of rabbit carotid arteries.

In rabbit carotid arteries intimal smooth muscle cell proliferations were induced by repeated local electrical stimulation of the artery wall. Oxygen uptake and lactate production of the proliferating tissue were determined in vitro and compared with the results obtained from nonstimulated arterial wall segments. Under the incubation conditions employed, oxygen consumption and lactate production of the proliferating tissue were 91.3 and 62.5 nmol x min-1 x mg-1 DNA, compared with the control values of 70.8 and 41.6 nmol x min-1 x mg-1 DNA. The DNA content of the proliferates and normal arterial wall tissue amounted to 9.6 and 12.0 microgram DNA x mg-1 dry weight. The results show that in proliferates obtained with the described procedure there is an increased capacity for ATP regenerating systems, respiration and glycolysis, indicating a modified function of the proliferating smooth muscle cells.

Significance of luminal plasma layer resistance in arterial wall oxygen supply

Previous analyses of the arterial wall oxygen supply system have assumed that a cell-free layer of plasma next to the endothelium is the major transport barrier in the lumen. Using a computer simulation, we have quantitatively tested this assumption. Our results show that oxygen diffusion gradients extend significantly into the flowing blood well beyond any plasma layer and that the major luminal transport resistance lies in the flowing blood and not in the plasma layer. The simulation was also employed to compute the effect of a reported 50% drop in plasma oxygen diffusivity. This rather large reduction did significantly lower oxygen levels within the arterial wall tissue. Whether such large reductions in diffusivity ever actually occur in human plasma is a subject of current controversy.

Computer simulation of the human thoracic aorta to evaluate the possible role of smoking in atherogenesis.

An impaired oxygen delivery to arterial wall tissue has been implicated as one factor in the atherogenic process (Getz et al., 1969). The arterial wall has a precarious O2 supply because its luminal side is completely avascular. Thus, the only supply of O2 to the avascular tissue zone is by diffusion over rather long distances from two sources: (1) the arterial blood flowing within the lumen and (2) the blood flowing within the vasa vasorum, the microcirculation of the outer portion of the wall.KeywordsArterial WallIntimal ThickeningHypoxic DamageCOHb LevelAtherogenic ProcessThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Consideration of atherosclerotic plaques as benign neoplasms

The monoclonal nature of atherosclerotic plaques, as well as their altered cell size, proliferation rate and function have led to the hypothesis that plaque tissue is analogous to benign tumors. To test this hypothesis, we have studied rates of DNA release by histologically-normal human arterial wall tissue and by early atherosclerotic plaques during incubation in a maintenance medium. No DNA was detected in media conditioned by normal arterial tissue after a 24 h incubation period, but plaque tissue (like benign tumors) released 10–100 ng DNA/ml during this period. These data offer additional support for the thesis that atherosclerotic plaques are similar to benign tumors.

Pathogenetic mechanisms in atherosclerosis

Four theories of atherogenesis are briefly reviewed and criticized: the degenerative, the thrombogenic, the platelet aggregation and the insudative theory. Evidence is presented in detail to suggest that a modified form of the insudative theory (1) accounts more satisfactorily than the other theories for the known association of risk factors with atherosclerosis and (2) allows one to understand how some of the more important risk factors operate at the level of the arterial wall. It is proposed that atherosclerotic plaques, and also certain extravascular lesions broadly associated with atherosclerosis (corneal arcus, xanthomas), arise because altered endothelial permeability allows certain reactive macromolecular plasma proteins (the plasma low density and very low density lipoproteins and fibrinogen, which are normally largely confined to the circulation) to permeate endothelium and interact with charged components of the connective tissue gel of the arterial wall or other tissues. The effect of hyperlipidemia, hyper-tension, arterial disease or injury upon this process, and the manner in which these factors interact, is examined in relation to experimental findings and clinical observations.

Deformation of the arterial vasa vasorum at normal and hypertensive arterial pressure.

In a previous paper, a numerical procedure (the finite element method) was presented for the structural analysis of soft biological structures possessing complex geometry and mechanical properties and undergoing large deformations. This method was used here to model a vas vasorum in an arterial cross-section subjected to physiological and hypertensive mean arterial pressure levels. The deformation of the lumen of the model vas vasorum was determined for two cases: an arteriole and a venule. Estimates of hydraulic resistance and flow rate for these model vasa vasorum were calculated and compared with experimental total flow rates in the vasa vasorum reported in the literature. The results indicate that prolonged abnormally elevated arterial pressure could constrict venules of the vasa vasorum thereby impairing arterial wall tissue nourishment. If no compensatory mechanisms exist, tissue degeneration and/or atherogenesis could occur.

Alterations with age in the viscoelastic properties of human arterial walls.

The circumferential incremental Young's modulus was measured in 59 major arteries of both "young" (less than 35 years of age) and "old" (greater than 35 years of age) subjects. Dynamic measurements of wall elasticity and viscosity were made which indicated a high viscosity in the femoral arteries. This was attributed to their high content of muscle. Although the "young" group showed, at any given pressure, an increasing wall stiffness towards the periphery, in "old" arteries, an opposite trend was found. When dimensional changes (radius and wall thickness) in the "old" group were considered it was apparent that at all sites the arterial wall tissue became weaker with age. Nevertheless, as a consequence of these dimensional changes the impedance characteristics of the old arterial tree still retained the nonuniformity (an increase towards the periphery) of the "young" which has considerable haemodynamic advantage.

Clinical studies on the brachial artery sphygmogram

The elasticity of the vascular wall has been the subject of many studies either with surgical or without surgical methods. The present author attempted to measure the elasticity of the arterial wall from the pulse wave curve recordable at the brachial artery and with a set of rather bold assumptions. Namely, the author assumed the arterial wall as a simple physical system with elasticity. Under this assumption the following equation will apply to the movement of the arterial wall: md2x/dt2=-Kx x=Sin ωt ω=2π/T T=2π√(m/K) where m : unit mass of the arterial wall tissue x : distance of the dislocation of a fixed point on the arterial wall vertical to the axis of the artery k : coefficient of elasticity T : period of sine wave The measurement of T will then allow the estimation of K, the coefficient of elasticity. Since, on the other hand, the velocity of the pulse wave propagation is related to the elasticity coefficient as follows : V∝√(p/K) there is another method of estimating the elasticity coefficient of the arterial wall. Methods Materials used consisted of three groups, (a) normal group, (b) arteriosclerotic group and (c) non-arteriosclerotic group consisting of cases with juvenile hypertension, nephritis and cardiac disease. The pulse wave was measured from the brachial artery by such arrangements that each pulse wave caused a corresponding change in the electrical capacity of the system which was presented to a condense microphone. At the same time, occlusion was applied 20cm distal to the point of the pulse wave recording by tighteing a vinyl-covered rubber band around the arm in order to measure the period of the reflected wave component (will be accentuated by occlusion) and measure the occlusion. Following this, the injection of TEAB or noradrenalin was performed and Pulse waves were recorded before and after injection (in this case, too, with and without occlusion). Throughout the course of these tests, simultaneous electrocardiograms were recorded by the third limb lead. The duration of time intervening between the R wave of electrocardiogram and the origin of ascending limb of the pulse wave gave the pulse wave arrival time. In this way the percentage change in pulse ware arrival time due to occlusion was also determined.