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An adventitia dependent regulation of the vascular smooth muscle tone has been described. However, if the adventitia plays an active role on arterial wall biomechanical behaviour and functions remains to be established. Our aim was to characterize the influence of adventitia on arterial wall mechanical properties and the arterial conduit and buffer functions.Ovine brachiocephalic arteries were studied in vivo (n = 8) and in vitro (with null tone) in a circulation mock (n = 8). Isobaric, isoflow and isofrequency studies were performed. In each segment, pressure and diameter waves were assessed before and after adventitia removal. From the arterial stress-strain relationship, we derived the elastic and the viscous modulus. The buffering and conduit functions were calculated using the Kelvin-Voigt's time constant and the inverse of the characteristic impedance, respectively.In in vivo studies arterial diameter decreased after adventitia removal (P0.05). Elastic and viscous modulus in in vivo studies were significantly higher in adventitia-removed arteries, compared with values in intact vessels (P0.05). This behaviour was not observed in in vitro experiments. An impairment of buffer and conduit functions was observed in vivo after adventitia removal (P0.05), while both functions remain unchanged in in vitro studies (P0.05).Arterial wall viscosity and elasticity were influenced by adventitia removal in in vivo studies, possibly by a smooth muscle-dependent mechanism, since it was not present in in vitro experiments. Adventitia would be involved in a physiological mechanism of arterial wall viscous and elastic properties regulation, that could influence arterial buffering and conduit functions.

Arteries are viscoelastic materials. Viscoelastic laws are fully characterized by measuring a complex modulus. Arterial mechanics can be described using stress-strain dynamic measurements applied to the particular cylindrical geometry. Most materials show an energy loss per cycle that increases steadily with frequency. By contrast, the frequency modulus response in arteries presents a frequency independence describing a plateau above a corner frequency near 4Hz. Traditional methods to fit this response include several spring and dashpot elements to model integer order differential equations in time domain. Recently, fractional derivative models proved to be efficient to describe rheological tissues, reducing the number of parameters and showing a natural power-law response. In this work a fractional derivative model with 4-parameter was selected to describe the arterial wall mechanics in-vivo. Strain and stress were measured simultaneously in an anaesthetized sheep. A fractional model was applied. The order resulted alpha=0.12, confirming the manifest elastic response of the aorta. The fractional derivative model proved to naturally mimic the elastic modulus spectrum with only 4 parameters and a reasonable small computational effort.

Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT–placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (η), inertial ( M ), and compliance ( C ) parameters, mean circumferential wall stress, viscous energy dissipation ( W D ), peak strain energy ( W St ), damping ratio (ξ= W D / W St ), and modeling isobaric indexes C Iso and W St(Iso) . The lack of VSM tonus isobarically increased wall stress and reduced η, C Iso , and damping ( P W D were greater in HT than in NT ( P P C Iso increased in HT-treated ( P W St increase, the arterial wall reacts increasing W D to maintain ξ. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.

The Favaloro University initiated the academic path in biomedical sciences in Buenos Aires, Argentina. As a very promising area, the biomedical world offers the integration between several domains, complementing medicine with engineering topics. The profile of the graduated students proved to be very versatile, allowing their instantaneous incorporation to the competitive market in this vast field. The university strategy is to concentrate basic science in the first 3 years and add the specific biological/medical concepts in the last 2 years. The students achieve a bachelor degree that integrates their knowledge in basic sciences. Afterwards, they attend a professional 2 year cycle, choosing between biomedical, physics and medical computing branches. The results proved to be effective in terms of professional and academic quality, market insertion and even the creation of promising seeds for future enterprises.

The viscoelastic and inertial properties of the arterial wall are responsible for the arterial functional role in the cardiovascular system. Cryopreservation is widely used to preserve blood vessels for vascular reconstruction but it is controversially suspected to affect the dynamic behaviour of these allografts. The aim of this work was to assess the cryopreservation's effects on human arteries mechanical properties. Common carotid artery (CCA) segments harvested from donors were divided into two groups: Fresh (n = 18), tested for 24-48 h after harvesting, and Cryopreserved (n = 18) for an average time of 30 days in gas-nitrogen phase, and finally defrosted. Each segment was tested in a circulation mock, and its pressure and diameter were registered at similar pump frequency, pulse and mean pressure levels, including those of normotensive and hypertensive conditions. A compliance transfer function (diameter/pressure) derived from a mathematical adaptive modelling was designed for the on line assessment of the arterial wall dynamics and its frequency response. Assessment of arterial wall dynamics was made by measuring its viscous (eta), inertial (M) and elastic (E) properties, and creep and stress relaxation time constant (tauC and tauSR, respectively). The frequency response characterization allowed to evaluate the arterial wall filter or buffer function. Results showed that non-significant differences exist between wall dynamics and buffer function of fresh and cryopreserved segments of human CCA. In conclusion, our cryopreservation method maintains arterial wall functional properties, close to their fresh values.

An arterial bypass might be either carried out with a venous segment or using a polytetrafluoroethylene (ePTFE) graft. Different patency rates were reported depending on the chosen method. Our objective was to compare the elastic properties of three different segment: A) expanded synthetic polytetrafluoroethylene (ePTFE) grafts, B) jugular veins, and C) systemic arteries (femoral artery). Pressure (P) and diameter signals were measured in six ovine venous, arterial, and ePTFE segments, mounted in a circulation mock and perfused at systemic pressure and stretch rate. Elastic modulus (E/sub inc/) was calculated at 100 mmHg using a pressure and diameter analysis. At systemic P level, both venous and ePTFE were suffer than the artery (p

Aim: We determined the wall mechanical response of the pulmonary artery (PA) to acute pulmonary hypertension induced pharmacologically and by an occlusion maneuver, to study the vascular response of the local segment and its influence in the whole pulmonary circulation. Methods: Pulmonary pressure and diameter were measured in six anaesthetized sheep under steady-state conditions. Transient hypertension in the PA was induced by phenylephrine (PHE) and a high pressure (HP) mechanical occlusion aimed at producing the same pulse and mean pressure responses. A viscoelastic arterial wall model was applied and the elastic (Epd) and viscous (μ) indexes were obtained. The μ/Epd ratio was adopted to quantify the damping performance of the arterial wall segment. The diastolic time constant was used as an indicator of the whole pulmonary buffering function. The systemic pressure was always measured. Results: The pulmonary mean, systolic and pulse pressure increases (P

To characterize the viscoelastic properties of the aorta and pulmonary arteries and the effects of vascular smooth muscle activation on arterial buffering function.Aortic and pulmonary artery pressure and diameter were measured in six anesthetized sheep under baseline conditions, and during arterial hypertension induced by mechanical vascular occlusion (passive), and i.v. phenylephrine (active). Arterial wall elasticity and viscosity were calculated, and buffering function was characterized: a) locally as the viscosity/elasticity ratio, and b) globally for each circuit, as the time-constant of ventricular relaxation.Viscoelasticity was higher in the aorta than in the pulmonary artery (p0.05), however, parietal buffering function was similar in both. Global buffering function was highest in the systemic circuit (p0.05). During passive hypertension, elasticity was significantly increased with no change in viscosity; this led to a significant reduction in local buffering function, and in global buffering function in each circuit. During active hypertension, viscosity increased (p0.05), while local and global buffering functions returned to baseline values.The viscosity/elasticity ratio was higher in the aorta than in the pulmonary artery, and arterial wall buffering function was similar in both vessels. Systemic global buffering function was higher than pulmonary circuit buffering function. Elasticity depends on intravascular pressure, whereas viscosity is a marker of the degree of smooth muscle activation. Smooth muscle activation may benefit the cardiovascular system by maintaining local and global buffering functions.

To characterize the buffering function of the pulmonary artery in vivo and to determine the role of vascular smooth muscle (VSM) activation in vessel wall elasticity.Pulmonary artery pressure and diameter were measured in 9 anesthetized sheep. Pulmonary artery hypertension was induced by mechanical occlusion of the pulmonary artery and by phenylephrine infusion (5 microg/kg/min) (PHE). Once the pressure-diameter loop was obtained, hysteresis was reduced to a minimum by increasing the modulus of viscosity. Elasticity was calculated as the first derivative of mean diastolic pressure assuming a purely elastic relation. Pulse wave velocity (PWV) and time constant (tau) were also obtained.Systolic, diastolic, mean and pulse pressures were similar during pulmonary artery hypertension and PHE infusion, but significantly higher in comparison to baseline conditions. Elasticity and diameter of the pulmonary artery increased significantly. In contrast, during VSM activation elasticity remained unchanged and diastolic diameter was reduced. PWV increased during both pulmonary artery hypertension and PHE infusion (p0.05); however, the increase during PHE infusion was smaller (15%) than during induced hypertension (33%). tau was significantly reduced during hypertension, but did not change during VSM activation.VSM activation may offset the deleterious effect of pulmonary artery hypertension on arterial wall stiffness by reducing elasticity and PWV. The VSM may modulate the Windkessel function in the pulmonary artery, preserving elasticity indexes during pulmonary artery hypertension.

The aim of this study was to evaluate and characterize arterial diameter and arterial wall viscoelastic variability. An animal study was performed on seven sheep instrumented in the brachycephalic artery. ECG, arterial diameter and pressure waveforms were simultaneously measured. Four different hemodynamic conditions were considered: 1) under anesthesia, 2) conscious steady state, 3) vascular smooth muscle (VSM) activation and 4) VSM relaxation. A system modeling identification approach was applied in order to estimate viscoelastic indexes. The linear autoregressive with exogenous input model (ARX) was applied to the single beat pressure-diameter data to assess the arterial system dynamics. The elastic and viscous indexes were derived from the identified ARX model. Arterial pressure and diameter, heart rate and viscoelastic indexes variability analysis were performed in the time and frequency domains. While systolic pressure and arterial diameter oscillation show a similar pattern to heart rate at all frequency bands in control condition, wall viscosity variability does not match with these parameters (p

The goal of this study was to determine the in vivo pulmonary arterial buffering function (BF) during acute and moderate pulmonary hypertension achieved by phenylephrine-induced smooth muscle activation. Pulmonary pressure (Konigsberg P7) and diameter (sonomicrometry) were measured in nine anesthetized sheep. Transit pulmonary arterial hypertension was induced by mechanical occlusion of the pulmonary artery (HP) and by phenylephrine infusion (5 microg/kg/min) (PHE). A viscoelastic Kelvin-Voigt model was used. By increasing the values of the viscous modulus, the pressure-diameter hysteresis area was reduced to a minimum in order to obtain the purely elastic pressure-diameter relationship. The elastic index (E) was calculated as the first derivative of the exponential model of the purely elastic pressure-diameter relationship at the mean pressure point. Systolic, diastolic, mean and pulse pressures were similar during HP and PHE, but significantly higher with regard to control steady state. In HP, E and arterial diameter (both its minimum and maximum values) increased significantly. In contrast, when pulmonary hypertension was induced by VSM activation, E was maintained concomitantly with pulmonary artery vasoconstriction. Pulmonary hypertension produced by occlusion of the pulmonary artery increases elasticity. Smooth muscle activation may offset the deleterious effect of pulmonary hypertension on arterial wall elasticity by reducing E and impeding arterial dilatation and collagen recruitment, maintaining BF during pulmonary hypertension.

The goal of this study was to determine the in vivo pulmonary arterial buffering function (BF) during acute and moderate pulmonary hypertension achieved by phenylephrine-induced smooth muscle activation.

In the present study a single beat evaluation of the system dynamics based on carotid pressure and diameter measurements is proposed. The influence of hypertension on the right common carotid artery wall properties was examined in 16 normotensive (NTA) control subjects and 14 patients with mild to moderate hypertension (HTA). Aortic diameter and pressure were sequentially measured during steady-state. The linear autoregressive moving average (ARMA) discrete time model was applied to the input-output (pressure-diameter) data to assess the arterial system dynamics. Using the inverse bilinear transformation, the elastic K/sup E/ viscous K/sub /spl eta// and inertial K/sub M/ indexes were derived from the model. A significant increase (P

Viscoelastic properties determine the dynamic behaviour of the arterial wall under pulsatile pressure and flow, suggesting time- or frequency-dependent responses to changes in wall stress and strain. The objectives of the present study were: (i) to develop a simplified model to derive simultaneously the elastic, viscous and inertial wall moduli; (ii) to assess Young's modulus as a function of frequency, in conscious, chronically instrumented dogs. Parametric discrete time models were used to characterise the dynamics of the arterial system based on thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements in control steady state and during activation of smooth muscle with the alpha-adrenoceptor agonist phenylephrine (5 microg kg(-1) min(-1), I.V.), in eight conscious dogs. The linear autoregressive model and a physically motivated non-linear model were fitted to the input-output (stress-strain) relationship. The aortic buffering function (complex Young's modulus) was obtained in vivo from the identified linear model. Elastic, viscous and inertial moduli were significantly increased from control state ((44.5 +/- 7.7) x 10(4) Pa; (12.3 +/- 4.7) x 10(4) Pa s; (0.048 +/- 0.028) x 10(4) Pa s(2) ) to active state ((85.3 +/- 29.5) x 10(4) Pa, P < 0.001; (22.4 +/- 8.3) x 10(4) Pa s, P < 0.05; (0.148 +/- 0.060) x 10(4) Pa s(2), P < 0.05). These moduli, obtained using the linear model, did not present significant differences compared with those derived using the non-linear model. In control conditions, the magnitude of the normalised complex Young's modulus was found to be similar to that reported in previous animal studies ranging from 1 to 10 Hz. During vascular smooth muscle activation, this modulus was found to be increased with regard to control conditions (P < 0.01) in the frequency range used in this study. The frequency-dependent Young's modulus of the aortic wall was obtained for the first time in conscious, unsedated dogs. The parametric modelling approach allows us to verify that vascular smooth muscle activation increases the elastic, viscous and inertial moduli with the advantage of being able to track their time evolution. Furthermore, under activation, the aortic wall remains stiff in the physiological frequency range, suggesting the impairment of the arterial buffering function. Experimental Physiology (2001) 86.4, 519-528.

Arterial vascular beds can be characterized considering the arterial segments in terms of their physical properties. These and other trees have an open structure based on repeated bifurcations, following fractal rules. Fractal dimension (FD) quantifies the time series complexity defined by its geometrical representation. Objective: To evaluate the arterial pressure and diameter time series in order to assess the influence of arterial tree structure in arterial pressure fractal dimension (FD). Methods: Simultaneous aortic pressure and diameter were measured in 14 conscious dogs. A pair of ultrasonic crystals, a pressure microtransducer and a pneumatic cuff occluder were positioned in the upper third of the descending aorta. Results: Total reflection induced by the occlusion maneuver decreased FD concomitant to the aortic stiffening and early wave reflection. Conclusion: Arterial pressure fractality is highly dependent on the arterial tree structure.

We read with interest Zanon et al. 's article1 published in the January 2009 issue, in which the left ventricle (LV)–arterial coupling was evaluated in heart failure patients, as the ratio between the arterial elastance (Ea) and the LV end-systolic elastance (Ees), before and after 1-year of cardiac resynchronization therapy (CRT). The authors found that an increased basal Ea/Ees quotient (afterload mismatch) would determine an increased probability to respond to CRT, when the response was evaluated using the quality-of-life (QoL) score or the LV end-systolic volume (ESV). Based in these results, the authors suggested that ‘the non-invasive quantification of the Ea/Ees may be proposed as an immediate, easy, and optimal tool for quantifying the effect of CRT in patients with heart failure’. The authors said, the Ea/Ees quotient ‘could be useful to select responders to this electrical therapy and to assess the cardiac performance over the time’. We agree with the authors in the Ea/Ees usefulness in the assessment of the cardiac performance. However, we have some questions and comments that we think should be considered at the time of proposing the use of the Ea/Es ratio as a tool to predict the response to CRT and should be taken into account when analysing the Zanon et al. work.1 The authors suggested that the Ea/Ees determination could be useful to quantify the CRT effects and to assess the cardiac performance over time. Accordingly, patients response to CRT was analysed as a function of the basal …

The influence of the renin-angiotensin system (RAS) on the aortic wall mechanical properties under angiotensin I converting enzyme inhibition (enalaprilat, 0.3 mg/kg iv) or angiotensin II receptor (AT1) blockade (E-3174, 1 mg/kg iv) was examined in eight normotensive and eight renovascular hypertensive conscious dogs. Aortic diameter (D; sonomicrometry)-pressure (P; microtransducer) hysteresis loops during steady state and during rapid distal aortic occlusion allowed (after hysteresis elimination) calculation of the aortic wall viscosity index, the purely elastic P-D relationship, and derivation into compliance-pressure curves. At the early stage ofrenovascular hypertension when activation of RAS is more pronounced, aortic wall stiffness and wall viscosity were increased as compared with normotensive states. Blood pressure remained unchanged in normotensive animals and was reduced during hypertension after antihypertensive treatments. In hypertensive animals, enalaprilat and E-3174 decreased viscosity index and shifted the compliance-pressure curve upward with respect to pretreatment conditions. In normotensive dogs, whereas E-3174 did not change the compliance-pressure curve and viscosity index, enalaprilat increased compliance and reduced viscosity index. We concluded that in normotensive dogs converting enzyme inhibition modifies arterial viscoelastic parameters by angiotensin-independent mechanisms that contribute to the modulation of the buffering function of large arteries.

The study of the rhythmic and nonrhythmic oscillations of the arterial blood pressure (ABP) was first described by Hales [19] two centuries ago. Twenty seven years later, Albrecht von Haller described fluctuations of the cardiac rhythm. In 1847, Carl Ludwig [31], by mean of continuous recordings of physiological events in horses and dogs, was able to graph the rhythmic fluctuations of the ABP. The motivation behind these experiments was to clarify the spontaneous behavior and to overcome the lack of interpretation for these oscillations. It is interesting to remind the first description relating an evident correlation with respiratory fluctuations, mainly because the ease of its visualization, both in laboratory animals and humans beings.

Abstract We compared the properties of common carotid and femoral arteries of 16 normotensive and 14 hypertensive men. Arterial pressure and diameter were recorded noninvasively in each vessel by tonometric and echotracking devices. The x - y composition of pressure and diameter waves provided the diameter-pressure hysteresis loop. The elastic diameter-pressure curve and wall viscosity index were deduced after hysteresis elimination. The compliance-pressure and distensibility-pressure curves were derived from the diameter-pressure curve, allowing the calculation of effective compliance and distensibility at the prevailing pressure of each subject and isobaric compliance and distensibility at the same standard pressure in all subjects. Systolic, diastolic, mean, and pulse pressures and diameters in each vessel were higher in the hypertensive than the normotensive group, except carotid pulse diameter, which did not differ. The carotid diameter-pressure, compliance-pressure, and distensibility-pressure curves did not differ between groups. In the carotid artery hypertensive patients had isobaric compliance and distensibility values similar to those of normotensive subjects, despite lower effective compliance ( P P P P P P

The advent of vascular diseases, such as hypertension and atherosclerosis, is associated to significant alterations in the physical properties of arterial vessels. Evaluation of arterial biomechanical behaviour is related to the assessment of three representative indices: arterial compliance, arterial distensibility and arterial stiffness index. Elasticity is the most important mechanical property of the arterial wall, whose natures is strictly non-linear. Intervention of elastin and collagen fibres, passive constituent elements of the arterial wall, is related to the applied wall stress level. Concerning this, appropriate tools are required to analyse the temporal dynamics of the signals involved, in order to characterize the whole phenomenon. Fractal geometry can be mentioned as one of those techniques. The aim of this study consisted on arterial pressure and diameter signals processing, by means of nonlinear techniques based on fractal geometry. Time series morphology was related to different arterial stiffness states, generated by means of blood flow variations, during experiences performed in vitro.

Previous experiences in animals showed a different behavior between the variability of pressure, arterial diameter and elasticity when they were registered for a couple of hours. To better understand arterial mechanics variability, we propose to measure simultaneously aortic pressure and diameter during 24 hours in a sheep. For that purpose, we developed a portable prototype device. It allows continuously recording physiological signals throughout the day and storing them in a solid state memory for later analysis. Pulse wave velocity and Peterson modulus were assessed beat-to-beat as arterial stiffness indexes. We identified 53,762 heart beats during 24 hours that were separated into 2 groups: below or above median mean pressure (71 mmHg). Mean diameter, pulse wave velocity and Peterson modulus increased for higher pressure values (p

Traditional risk factors are involved in the development of coronary artery disease (CAD), but geometrical risk factors have also proved to be determinant. In this work we present a new method to construct a 3D map of the left coronary artery tree using CT image processing and skeletonization techniques. We computed cumulative length-volume functions through the coronary tree bifurcations and also the relationships between total tree volumes, total length, number of segments and bifurcations with respect to the presence and severity of atherosclerotic plaques. A total of 65 patients, 40 with and 20 without CAD were recruited. We found more vascular segments and bifurcations per patient in the CAD group. Accordingly, total cumulative length was longer in CAD patients (p

Increased arterial stiffness is associated with an increased risk of cardiovascular events. Estimation of arterial stiffness using local pulse wave velocity (PWV) promises to be very useful for noninvasive diagnosis of arteriosclerosis. In this work we estimated in an instrumented sheep, the local aortic pulse wave velocity using two sonomicrometry diameter sensors (separated 7.5 cm) according to the transit time method (PWVTT) with a sampling rate of 4 KHz. We simultaneously measured aortic pressure in order to determine from pressure-diameter loops (PWVPDLoop), the true local aortic pulse wave velocity. A pneumatic cuff occluder was implanted in the aorta in order to compare both methods under a wide range of pressure levels. Mean pressure values ranged from 47 to 101 mmHg and mean proximal diameter values from 12.5. to 15.2 mm. There were no significant differences between PWVTT and PWVPDLoop values (451?43 vs. 447?48 cm/s, p = ns, paired t-test). Both methods correlated significantly (R = 0.81, p

Endothelial function can be assessed non-invasively with ultrasound, analyzing the change of brachial diameter in response to transient forearm ischemia. We propose a new technique based in the same principle, but analyzing a continuous recording of carotid-radial pulse wave velocity (PWV) instead of diameter. PWV was measured on 10 healthy subjects of 22±2 years before and after 5 minutes forearm occlusion. After 59 ± 31 seconds of cuff release PWV decreased 21 ± 9% compared to baseline, reestablishing the same after 533 ± 65 seconds. There were no significant changes observed in blood pressure. When repeating the study one hour later in 5 subjects, we obtained a coefficient of repeatability of 4.8%. In conclusion, through analysis of beat to beat carotid-radial PWV it was possible to characterize the temporal profiles and analyze the acute changes in response to a reactive hyperemia. The results show that the technique has a high sensitivity and repeatability.

Ergometric exercise stress tests (EST) give important information about the cardiovascular (CV) response to increased demands. The expected EST-related changes in variables like blood pressure and heart rate are known, but those in the arterial biomechanics are controversial and incompletely characterized. In this context, this work aims were to characterize the regional and local arterial biomechanical behaviour in response to EST; to evaluate its temporal profile in the post-EST recovery phase; and to compare the biomechanical response of different to EST. Methods: In 16 non-trained healthy young subjects the carotid-femoral pulse wave velocity and the carotid, femoral and brachial arterial distensibility were non-invasively evaluated before (Rest) and after EST. Main results: The EST resulted in an early increase in the arterial stiffness, evidenced by both, regional and local parameters (pulse wave velocity increase and distensibility reduction). When analyzing conjunctly the different post-EST recovery stages there were quali-quantitative differences among the arterial local stiffness response to EST. The biomechanical changes could not be explained only by blood pressure variations.

Early investigators found contradictory evidence that vascular smooth muscle activation reduces the elastic modulus of the arterial wall under isotonic conditions but increases it under isometric conditions, concomitant with increased pulse-wave velocity. We examined the individual contributions of aortic constituents to the elastic modulus of the aortic wall to determine if isobaric analysis produces an accurate assessment of vascular smooth muscle activation. We used a modified Maxwell model assuming an incremental elastic modulus (Einc) composed of the elastic modulus of elastin fibers (EE), the elastic modulus of collagen fibers (EC) affected by the fraction of collagen fibers (fC) recruited to support wall stress, and the elastic modulus of the vascular smooth muscle (ESM) according to the following formula: Einc = EE+EC x fC+ESM.Einc was assessed in eight conscious dogs using descending thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements. Stress-strain relations in the control state and during activation of smooth muscle by continuous administration of phenylephrine (5 micrograms.kg-1 x min-1) were obtained by transient occlusions of the descending aorta and inferior vena cava. Results were as follows: EE was 4.99 +/- 1.58 x 10(6) dynes/cm2 (mean +/- SD), and EC was 965.8 +/- 399.8 x 10(6) dynes/cm2, assessed during the control state. Phenylephrine administration increased the theoretical pulse-wave velocity (Moens-Korteweg equation) from 5.25 +/- 1.03 m/s during the control state to 7.57 +/- 2.53 m/s (P < .005). Active muscle exhibited a unimodal stress-strain curve with a maximum stress of 0.949 +/- 0.57 x 10(6) dynes/cm2 at a corresponding strain value of 1.299 +/- 0.083. The maximum value observed corresponded, on the pressure-diameter curve of the active artery, to a pressure of 234.28 +/- 46.6 mm Hg and a diameter of 17.94 +/- 1.6 mm. The maximum ESM derived from the stress-strain relation of the active muscle was 8.345 +/- 7.56 x 10(6) dynes/cm2 at a strain value of 1.283 +/- 0.079. This point was located at 208.01 +/- 40.8 mm Hg and 17.73 +/- 1.41 mm on the active pressure-diameter curve. During activation of vascular smooth muscle, Einc decreased (P < .05) when plotted against internal pressure but increased (P < .05) when plotted against strain, over the operative range.(ABSTRACT TRUNCATED AT 400 WORDS)

Objective: The aim was to assess the influence of the renin-angiotensin system on the geometrical and elastic properties of the aorta in conscious dogs, using a model of renovascular hypertension, and to examine the effects of inhibition of the system by the angiotensin converting enzyme inhibitor spirapril. Methods: The aortic elastic behaviour in response to renovascular hypertension was studied in 15 conscious dogs instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. Renovascular hypertension was induced by surgical occlusion of one renal artery and stenosis of the other. One day after renal surgery, dogs were randomly assigned to two groups receiving for two months either the new angiotensin converting enzyme inhibitor spirapril (n=8) or a placebo capsule (n=7). The two groups of dogs were compared to a control group of normotensive dogs (n=7). After two months of treatment the elastic properties of the aorta were studied by computation of the beat to beat pressure-diameter hysteresis loops obtained during transient increase of pressure induced by bolus doses of angiotensin. The aortic pressure- diameter (P-D) relationship, obtained over a wide range, was fitted by an exponential fit (P=α·eβD), where β is the stiffness index. A decomposition of the P-D curve according to a biphasic model of the parallel arrangement of elastin and collagen enabled two pressure-diameter elastic moduli to be obtained, one representing the resistance to stretch at low pressure levels (elastic fibres and smooth muscle), and the other representing the resistance to stretch at the highest pressures (collagen fibres). Results: The pressure-diameter curve of the placebo group was shifted to the left compared to the curves of the control and spirapril groups, showing that renovascular hypertension was associated with isobaric reduction of aortic diameter. The stiffness index β was higher (p

We studied the aortic elastic behavior in response to vitamin D3-induced accelerated calcinosis in conscious dogs chronically instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. The two functional phases of the elastic segmental properties of the aorta in vivo were discriminated by computation on a beat-by-beat basis from the phasic pressure-diameter (P-D) hysteresis loops in basal conditions and during the transient state of a wide range of pressures obtained mechanically (aortic occlusion) or pharmacologically (angiotensin bolus). The overall P-D curve formed by all P-D hysteresis loops was comprised of two linear relations according to a model that assumes that only elastin is stretched at lower pressures, whereas both elastin and collagen are stretched at higher pressures. The slope of the first linear portion of the P-D curve was considered as the elastin P-D elastic modulus, and the slope of the curve obtained by subtraction between the P-D curve and the extrapolation of the elastin straight line was assumed to be the collagen P-D elastic modulus. After vitamin D3-induced calcinosis, the elastin elastic modulus was unaffected, whereas the collagen elastic modulus decreased significantly during occlusion maneuvers (58.6%, p less than 0.01) and during bolus injections of angiotensin (37.2%, p less than 0.05). The collagen elastic modulus correlated with the serum calcium concentration (r = -0.65, p less than 0.001) and with the aortic pulse pressure (r = 0.51, p less than 0.01), and this relation persisted at constant heart rate. Histopathologic analysis evidenced calcium-depositing elastic lamina, focal disappearance of collagen, and rupture of elastic fibers. The present study shows that accelerated, severe, experimental calcinosis-inducing calcium deposition inside the large artery walls is accompanied by a clear-cut paradoxical reduction in arterial rigidity that is mainly due to functional and structural modification of collagen elasticity.

The elastic behavior of total elastin (EE) and collagen (EC) and the recruitment of collagen fibers (FC) supporting wall stress at a given transmural pressure level were assessed in seven conscious dogs using descending thoracic aortic pressure (microtransducer) and diameter (sonomicrometer) measurements. Stress-strain relationships values calculated at control and during bolus administration of angiotensin and nitroglycerin enabled quantification of angiotensin and nitroglycerin enabled quantification of elastic moduli of elastin (EE = 4.868 +/- 1.753 x 10(6) dyn/cm2; means +/- SD) and collagen (EC = 1,306 +/- 637 x 10(6) dyn/cm2) according to a biphasic model of elastin and collagen parallel arrangement. The FC was found to be 6.1 +/- 2.6% at a pressure level of 118 +/- 16 mmHg. Values for EE and EC were similar to those reported in in vitro studies and showed scarce variability. This approach provides a quantitative evaluation of elastin and collagen moduli in conscious animals and also permits the evaluation of FC, which may be of interest in studies of connective tissue diseases involving the aortic wall.

To the Editor: In the November 2003 issue of Stroke , Vernhet and colleagues reported a clinical analysis of wall mechanics in stented extracranial carotid arteries, and they concluded that stenting of these arteries induces a compliance mismatch between the native and the stented artery. Additionally, the authors observed a significant decrease in the distensibility coefficient of the stented region.1 These are remarkable findings and are in accordance with others, in which the mismatch observed between the mechanical properties of the prosthetic graft and that of the adjacent native artery is conducive to the development of distal anastomotic intimal hyperplasia.2 However, the study of Vernhet and coworkers did not reflect wall mechanics of stented carotid arteries as is suggested in the title. A complete mechanical study involves a characterization of geometric, elastic, and viscous properties of the arteries that can be performed …

We describe a technique for the production of acute progressive right ventricular failure in experimental animals that mimics the hemodynamic characteristics of right ventricular failure found in some patients being weaned from extracorporeal circulation after surgical repair of left ventricular abnormalities. The technique combines three alterations of right ventricular state: excision of the tricuspid valve, ventriculotomy, and ligation of the right coronary artery. Seven control dogs died within 3 hours after this intervention. Death was due to low cardiac output as a result of low left atrial and pulmonary arterial pressures. Right atrial pressure was high. Use of a right ventricular assist device in an additional seven dogs to pump blood from the right atrium to the pulmonary artery confirmed good preservation of left ventricular function by reestablishing adequate left ventricular filling pressure. All seven dogs survived for more than 3 hours. The validity of the technique in restricting failure principally to the right ventricle was thus demonstrated.

The aortic elastic behavior has been studied in conscious dogs chronically instrumented with a pressure microtransducer and two ultrasonic crystals. Pressure and diameter measurements were analyzed in terms of their mean values and systolic-diastolic variations, enabling calculation of Peterson elastic modulus, and were displayed in the x-y form to obtain pressure diameter hysteresis loops. After recovery from surgery and under autonomic blockade, intravenous perfusions of angiotensin, norepinephrine, and epinephrine were made at incremental steps of doses until steady-state pressure-diameter changes were achieved. The slopes of the positive pressure-diameter correlations obtained at each dose of the same vasoactive substance were higher for angiotensin than norepinephrine (p less than 0.01) and epinephrine (p less than 0.001) and were higher for norepinephrine than epinephrine (p less than 0.05). Similarly, the slopes of the elastic modulus to mean pressure relation were significantly lower for angiotensin than for norepinephrine (p less than 0.05) and epinephrine (p less than 0.001) and were significantly lower for norepinephrine than epinephrine (p less than 0.001). Thus, at the same transmural pressure, the distension and stiffness of the aorta were lower and higher with epinephrine than with norepinephrine, respectively, and with norepinephrine than with angiotensin suggesting different potencies of these drugs in terms of smooth muscle activation in the aorta.

Using three intraventricular diameter signals obtained from ultrasonic distance gauges and applying the general ellipsoid model to the left ventricle, it was possible to obtain the left ventricular volume signal Implanting a miniature transducer in the left ventricle the pressure signal was attained. With these two signals the pressure-volume diagrams were constructed on line, and ventricular function during load manoeuvres could be studied from them. Because the whole process was done on line, using a microcomputer, the performance of the left ventricle to load manoeuvres in different conditions could be seen instantly.

OBJECTIVESWe sought to investigate wall shear rate (WSR) and brachial artery diameter (BAD) changes simultaneously and to determine whether any gender differences exist in arterial reactivity.BACKGROUNDWall shear rate/stress and arterial reactivity are rarely assessed at the same time. Furthermore, flow-mediated vasoconstriction has received less attention than flow-mediated vasodilation in humans.METHODSA new noninvasive evaluation of WSR in the brachial artery, using multigated, pulsed Doppler velocimeter and a double-transducer probe moved and fixed by a robotic system, was developed.RESULTSThe validity of the system was tested in vitro with calibrated tubes and showed a high correlation (r = 0.98, p < 0.001). In 10 men and 10 women of similar age, induction of low and high shear rates by forearm occlusion produced significant vasoconstriction and vasodilation, respectively. The time lag for maximal BAD changes was 3 min for vasoconstriction and 1 min for vasodilation. A greater half-time for vasodilation (96 ± 6 for men and 86 ± 12 s for women) than for shear rate (31 ± 5 s for men and 34 ± 4 s for women) was observed after discontinuation of occlusion. Relative BAD was correlated with WSR changes, showing a significantly higher slope in women than in men (p < 0.01). Moreover, a larger normalized arterial diameter per shear rate was observed for vasoconstriction (p < 0.01) and vasodilation (p < 0.01) in women than in men.CONCLUSIONSShear-mediated arterial vasodilation and vasoconstriction were more pronounced in women than in men, suggesting different gender-related sensitivity in the regulation of large-artery vascular tone.