Dynamic versus Static Compliance of the Carotid Artery in Living Wistar-Kyoto Rats

Abstract

Arteries, when they are subjected in vitro to cyclic loading and unloading, are reported to be stiffer than in static conditions and to be poorly influenced by changes in vasomotor tone. However, such parameters have never been studied in living animals. This study used very high resolution echotracking technics to evaluate pulsatile changes of carotid blood pressure and diameter and the resulting dynamic pressure-cross-sectional (CSA) curve in anesthetized Wistar-Kyoto rats before and following changes of arteriolar vasomotor tone produced by vasoconstrictive [phenylephrine, L-N^G nitro-arginine (LNA)] or vasodilating (hydralazine, nitroprusside) agents. Phenylephrine and LNA caused a progressive upward shift of the pressure-CSA curve toward significantly higher values of mean blood pressure and diameter. Since the two vasoconstrictive agents produced exactly the same arterial hemodynamic pattern, their effects may be considered as ‘passive’, i.e. predominantly due to the mechanical effect of pressure distension. From this observation, a simple model was validated, permitting evaluation in vivo of the passive static properties of the pressure-CSA curve from the relationship between mean arterial diameter and mean arterial pressure at the various steady states produced by the two vasoconstrictive agents. This static relationship had a significantly steeper slope than the corresponding dynamic relationships determined for the same steady-state mean arterial pressures. With hydralazine, a downward shift of the pulsatile pressure-CSA curve was obtained, with exactly the same characteristics as for phenylephrine and LNA, but within lower ranges of blood pressure and with a corresponding decrease in arterial diameter. In contrast, nitroprusside shifted the pulsatile pressure diameter curve toward both lower values of blood pressure and higher values of arterial diameter, thus indicating an active change in arterial tone. At any given value of mean blood pressure and arterial diameter, operational pulsatile compliance was significantly higher with sodium nitroprusside than with hydralazine. This study provides evidence that in living rats (1) the described static carotid pressure-diameter curve has a significantly steeper slope than the corresponding dynamic curve for the same mean arterial pressure, (2) for the same mean arterial pressure and diameter, sodium nitroprusside has a significantly higher dynamic compliance than hydralazine, implicating the role of nonhemodynamic factors in the stiffness changes, and (3) vasomotor tone influences markedly the dynamic pressure-diameter (or CSA) curve within intermediate and lower blood pressure ranges through active mechanisms involving the GMP cyclic pathway.

Association between 24-hour ambulatory heart rate and arterial stiffness

“…Bergel et al 19 have shown in in vitro studies that aortic dynamic elastic modulus is larger than static modulus. In anesthetized normotensive rats, Glaser et al 20 showed that dynamic compliance was lower than static compliance at any given mean arterial pressure. When tachycardia is induced by atrial pacing, PWVcf (m/s) 10.5 ± 2.2 13.4 ± 3.8 ‡ 11.6 ± 2.8°12.7 ± 2.9 †…”

Assessment of the viscosity of the pulmonary artery wall

“…In reality, however, part of the energy that corresponds to viscous deformation is dissipated within the arterial wall. Wall viscosity reduces the efficiency of heart/vessel coupling, and may place extra load on the ventricle [3].Wall viscosity is responsible for the difference that exists between the static (Dst) and dynamic distensibility (Ddyn) of a given vessel [1,2,4,5]. Under static conditions, the change in diameter in response to a given change in distending pressure is determined only by the elastic properties of the vessel wall.…”

“…Dst The arterial wall responds to stress through both elastic and viscous behaviour, the former being related to the elastin and the latter to the collagen and smooth muscle content of the vessel wall [1,2]. During systole, the elastic behaviour of the arterial wall allows its diameter to increase proportionally to pressure; in the case of a purely elastic arterial wall, the total amount of energy stored would be released during diastole.…”

“…Wall viscosity is responsible for the difference that exists between the static (Dst) and dynamic distensibility (Ddyn) of a given vessel [1,2,4,5]. Under static conditions, the change in diameter in response to a given change in distending pressure is determined only by the elastic properties of the vessel wall.…”

“…The greater the wall viscosity, the greater the difference between Dst and Ddyn. Dst has been found to be considerably higher than Ddyn in systemic arteries, the difference being accounted for by wall viscosity [1,2,4,5].…”