Influence of Flow and Pressure on Wave Propagation in the Canine Aorta

Abstract

Data on wave speed acquired from 20 anesthetized dogs showed that the thoracic aorta was essentially nondispersive for small artificially generated pressure waves traveling in the downstream or the upstream direction and having frequencies between 40 and 120 Hz. The amplitude of these waves decayed exponentially with the distance traveled. The attenuation was independent of frequency and pressure if the distance was measured in wavelengths. The logarithmic decrement of the downstream waves ranged between 0.7 and 1.0, whereas that of the retrograde waves was between 1.3 and 1.5. The discrepancy in the attenuation for the two directions appeared to be due to the taper of the thoracic aorta. Simultaneous measurements of the transmission times of waves traveling downstream and upstream indicated that small pressure perturbations were convected with a speed that was approximately equal to the mean flow velocity. The speed of such perturbations depended strongly on the aortic pressure level at which they were generated. For normal pressure pulses generated by the heart, the speed of small perturbations at systole might be 30% higher than that at diastole. Theoretical studies have shown that such changes in wave speed due to variations in pressure and flow produce marked nonlinear effects in hemodynamics. KEY WORDSnonlinear properties of aorta phase velocity convection of pressure signals wave transmission characteristics dissipative mechanisms elastic behavior of blood vessels retrograde wavesFrom the

Altered Dependence of Aortic Pulse Wave Velocity on Transmural Pressure in Hypertension Revealing Structural Change in the Aortic Wall

“…To our knowledge, this is the first study to have examined the relation between aPWV and TMP in vivo in man using a direct mechanical approach to modulate TMP, and the results reveal structural change in the properties of the aorta in hypertensive compared with normotensive subjects that cannot be appreciated from simple resting measures of aPWV. In normotensive subjects, the results demonstrate an increase in aPWV with increasing TMP, replicating results observed during mechanical manipulation of blood pressure in the canine aorta 6 and increase in blood pressure in humans achieved by infusion of angiotensin II. 10,26 By contrast, in hypertensive subjects, aPWV is seen to show little variation with TMP.…”

“…3,4 By contrast, aPWV is closely associated with concurrent levels of blood pressure 5 implicating hypertension in the etiology of aortic stiffening. However, it is unclear whether the relation of aPWV to blood pressure is simply because of the aorta becoming stiffer as it is stretched by a higher transmural distending pressure (TMP, usually equal to intra-aortic blood pressure) 6 or whether it results from a structural change in the aortic wall associated with and contributing to a sustained elevation in blood pressure (ie, hypertension). Previous attempts to address this question by obtaining indirect estimates of isobaric stiffness have yielded conflicting results.…”

Wave dissipation in flexible tubes in the time domain: In vitro model of arterial waves

“…The concurrence of the degree of dissipation demonstrates that wave dissipation in uniform elastic tubes has a strong similarity between the forward and backward directions. This finding agrees with that of Histand and Anliker (1973). They found that the ''wave travelling in either direction exhibited similar exponential decay patterns for their amplitudes''.…”

Acute Reduction of Blood Pressure by Nitroglycerin Does Not Normalize Large Artery Stiffness in Essential Hypertension

“…9,10 An acute elevation of blood pressure results in increased arterial stiffness in both animal models and in human subjects. 9,11,12 However, in hypertensive subjects it is not clear whether increased stiffness occurs as a result of elevated blood pressure or whether there is an intrinsic change in the elasticity of the arterial wall so that, when compared at the same operating pressure, it is stiffer than that in normotensive subjects. Previous studies to address this issue have examined the relationship of arterial pressure to diameter of the common carotid artery throughout the cardiac cycle with extrapolation to a common pressure.…”