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AP • V/AV • h (mm Hg/cm) (fig. 7)

Nowadays, most of these indices are measured non-invasively in vivo using echo-Doppler techniques with high resolution and high degree of reproducibility, particularly for D, AD and h. The most important difficulty is BP measurement, which may require local tonometry. The latter then requires calibration, which remains a difficult problem to resolve.

P = Pressure; D = diameter; V = volume; h = wall thickness; t = time.

1 These indices are site-specific and vary with distending pressure (fig. 7). They may be measured in vivo (active properties in the presence of VSM tone) or in vitro (or even in vivo, in situ) (passive properties after poisoning VSM cells).

Nowadays, most of these indices are measured non-invasively in vivo using echo-Doppler techniques with high resolution and high degree of reproducibility, particularly for D, AD and h. The most important difficulty is BP measurement, which may require local tonometry. The latter then requires calibration, which remains a difficult problem to resolve.

P = Pressure; D = diameter; V = volume; h = wall thickness; t = time.

1 These indices are site-specific and vary with distending pressure (fig. 7). They may be measured in vivo (active properties in the presence of VSM tone) or in vitro (or even in vivo, in situ) (passive properties after poisoning VSM cells).

apoptotic properties [3, 10]; The distribution of these phenotypes is mainly influenced by age, by the location within the vascular tree, and the presence of underlying pathological factors. VSM contractile properties, which are mainly expressed in muscular arteries and arterioles, are responsible for the active mechanical properties of these vessels [1-3]. Changes in VSM tone may occur either directly or through signals arising from endothelial cells. Endothelium is a source of substances, particularly nitric oxide (NO), and of signal transduction mechanisms [11], that necessarily influence the biophysical properties of arteries and are defined according to the same mathematical formulas as passive mechanical properties (table 1; fig. 7) [1-3]; Many of these signals are influenced by blood flow through the mechanism of endothelium-dependent flow dilatation, which is observed for vessels of all sizes (muscular or musculo-elastic). In contrast, the role of mediators arising from endothelium predominates in muscular distal arteries and arterioles [3, 11, 12]; The wall-to-lumen ratio of such vessels is influenced by the local differential effects of NO and other vasodilating (bradykinin-prostaglandins) or vasoconstricting (norepi-nephrine, angiotensin, endothelin) compounds.

Fig. 7. Schematic representation of the pressure-volume relationship in CV structures with different incremental elastic modulus (Einc: intrinsic stiffness ofbiomaterials) (see table 1). Increasing Einc shifts the pressure-volume (or diameter) curve to the left, increasing the pressure effect of volume changes [1-3]. Note that each pressure-volume curve is curvilinear, due to the role of elastin at low pressure and collagen at high pressure. Thus, the slope dP/d V of the pressure-volume relationship is reduced when pressure increases, and characterizes, at each given pressure, the elasticity of the system (called also compliance or distensibility: see table 1). When the material of the arterial wall is changed (i.e., when Einc changes from position 1 to position 2; see table 1), the pressure-volume curve is reset [1-3].

Fig. 7. Schematic representation of the pressure-volume relationship in CV structures with different incremental elastic modulus (Einc: intrinsic stiffness ofbiomaterials) (see table 1). Increasing Einc shifts the pressure-volume (or diameter) curve to the left, increasing the pressure effect of volume changes [1-3]. Note that each pressure-volume curve is curvilinear, due to the role of elastin at low pressure and collagen at high pressure. Thus, the slope dP/d V of the pressure-volume relationship is reduced when pressure increases, and characterizes, at each given pressure, the elasticity of the system (called also compliance or distensibility: see table 1). When the material of the arterial wall is changed (i.e., when Einc changes from position 1 to position 2; see table 1), the pressure-volume curve is reset [1-3].

In muscular arteries, dilators such as nitroglycerine cause a large degree of dilation but little change or even an increase in arterial stiffness, whereas constrictors seem to have an opposite effect. Such hemodynamic profiles can be explained on the basis of models connecting VSM cells to the stiff collagen and less stiff elastin fibers [2]. It has been suggested that VSM cells are in series with collagen but in parallel with elastin [2]. Hence, muscular contraction makes an artery stiffer as well as more narrow, whereas muscular relaxation makes the artery less stiff as well as wider. Nevertheless, the latter change may not be apparent if collagenous fibers are modified by the passive increase in diameter.

Finally, through their dilating properties, arteriolar vessels may contribute to change the pattern of wave reflections. Reflection sites are located at any discontinuity of ECM and/or VSM cells. The reflectance properties of the arterial and arteriolar system are nowadays the subject of emerging research.

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