Seven classic and recently proposed methods used for the estimation of total arterial compliance have been evaluated for their accuracy and applicability in different physiological conditions. The pressure and flow data are taken from a computer model that provides realistic simulations of the nonlinear-distributed systemic arterial tree. Besides the great flexibility in simulating different physiological or pathological cases, the major advantage of the computer model is that it allows precise knowledge of the pressure-dependent total arterial compliance, which is the variable of interest. The results show that the methods based on the two-element windkessel (WK) model are more accurate than those based on the three-element WK model. The classic exponential decay and the diastolic area method yield essentially similar results, and their compliance estimates are accurate within 10% except at high heart rates. The later part of diastole, i.e., from the time that the systolic pressure wave has reached all peripheral beds, gives the best results. The newly proposed two-area and pulse pressure methods, both based on the two-element WK model, are accurate (errors in general < 10%) and can be applied to other locations in the arterial tree where the decay time and area method cannot. Methods based on the three-element WK model consistently overestimate total arterial compliance (> or = 25%). The errors in the methods based on the three-element WK model arise from the fact that the input impedance in that model deviates significantly from the true input impedance at low frequencies. The strong dependence of compliance on pressure (elastic nonlinearity) does not invalidate the compliance estimates.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial wall stresses are thought to be a major determinant of vascular remodeling both during normal growth and throughout the development of occlusive vascular disease. A completely physiologic mechanical model of the arterial wall should account not only for its residual strains but also for its structural nonhomogeneity. It is known that each layer of the artery wall possesses different mechanical properties, but the distribution of residual strain among the different mechanical components, and thus the true zero stress state, remain unknown. In this study, two different sets of experiments were carried out in order to determine the distribution of residual strains in artery walls, and thus the true zero stress state. In the first, collagen and elastin were selectively eliminated by chemical methods and smooth muscle cells were destroyed by freezing. Dissolving elastin provoked a decrease in the opening angle, while dissolving collagen and destroying smooth muscle cells had no effect. In the second, different wall layers of bovine carotid arteries were removed from the exterior or luminal surfaces by lathing or drilling frozen specimens, and then allowing the frozen material to thaw before measuring residual strain. Lathing material away from the outer surface caused the opening angle of the remaining inner layers to increase. Drilling material from the inside caused the opening angle of the remaining outer layers to decrease. Mechanical nonhomogeneity, including the distribution of residual strains, should thus be considered as an important factor in determining the distribution of stress in the artery wall and the configuration of the true zero stress state.

The non-linear elastic response of arteries implies that their mechanical properties depend strongly on blood pressure. Thus, dynamic measurements of both the diameter and pressure curves over the whole cardiac cycle are necessary to characterise properly the elastic behaviour of an artery. We propose a novel method of estimating these mechanical properties based on the analysis of the arterial diameter against pressure curves derived from ultrasonic and photoplethysmographic measurements. An ultrasonic echo tracking device has been developed that allows continuous recording of the internal diameter of peripheral arteries. It measures the diameter 300 times per second with a resolution of 2.5 microns. This system is linked to a commercially available light-plethysmograph which continuously records the finger arterial pressure (0.25 kPa accuracy). Because of the finite pulse wave velocity, the separation between the diameter and the pressure measurement sites causes a hysteresis to appear in the recorded diameter-pressure curve. Using a model based on haemodynamic considerations, the delay between the diameter variations and the finger arterial pressure is first eliminated. As the pulse wave velocity depends on the pressure, the delay is determined for each pressure value. The relationship between pressure and diameter is then described by a non-linear mathematical expression with three parameters, which best fits the recorded data. The dynamic local behaviour of the vessel is fully characterised by these parameters. Compliance, distensibility and pulse wave velocity can then be calculated at each pressure level. Thus, the mechanical behaviour of peripheral human arteries can now be characterised non-invasively over the pressure range of the whole cardiac cycle. The results obtained in vivo on human radial and brachial arteries show that a thorough analysis of the compliance-pressure curves and their modifications (curving, shift) is needed in order to compare two different vessels in a meaningful way.

Leading edge protrusion is one of the critical events in the cell motility cycle and it is believed to be driven by the assembly of the actin network. The concept of dendritic nucleation of actin filaments provides a basis for understanding the organization and dynamics of the actin network at the molecular level. At a larger scale, the dynamic geometry of the cell edge has been described in terms of the graded radial extension model, but this level of description has not yet been linked to the molecular dynamics. Here, we measure the graded distribution of actin filament density along the leading edge of fish epidermal keratocytes. We develop a mathematical model relating dendritic nucleation to the long-range actin distribution and the shape of the leading edge. In this model, a steady-state graded actin distribution evolves as a result of branching, growth and capping of actin filaments in a finite area of the leading edge. We model the shape of the leading edge as a product of the extension of the actin network, which depends on actin filament density. The feedback between the actin density and edge shape in the model results in a cell shape and an actin distribution similar to those experimentally observed. Thus, we explain the stability of the keratocyte shape in terms of the self-organization of the branching actin network.

We derived and tested a new, simple, and accurate method to estimate the compliance of the entire arterial tree and parts thereof. The method requires the measurements of pressure and flow and is based on fitting the pulse pressure (systolic minus diastolic pressure) predicted by the two-element windkessel model to the measured pulse pressure. We show that the two-element windkessel model accurately describes the modulus of the input impedance at low harmonics (0-4th) of the heart rate so that the gross features of the arterial pressure wave, including pulse pressure, are accounted for. The method was tested using a distributed nonlinear model of the human systemic arterial tree. Pressure and flow were calculated in the ascending aorta, thoracic aorta, common carotid, and iliac artery. In a linear version of the systemic model the estimated compliance was within 1% of the compliance at the first three locations. In the iliac artery an error of 7% was found. In a nonlinear version, we compared the estimates of compliance with the average compliance over the cardiac cycle and the compliance at the mean working pressure. At the first three locations we found the estimated and "actual" compliance to be within 12% of each other. In the iliac artery the error was larger. We also investigated an increase and decrease in heart rate, a decrease in wall elasticity and exercise conditions. In all cases the estimated total arterial compliance was within 10% of mean compliance. Thus, the errors result mainly from the nonlinearity of the arterial system. Segmental compliance can be obtained by subtraction of compliance determined at two locations.