Biomedical subjects

Daniel Bia

Publications and source records attributed to Daniel Bia.

8 recordsLinked to original sources

PubMed2006

Improved right ventricular-vascular coupling during active pulmonary hypertension.

Right ventricular adaptation to pulmonary hypertension (PH) is an important prognostic factor. Pulmonary artery (PA) smooth muscle activation attenuates arterial dysfunction during acute PH. We investigated the role of the pulmonary artery vascular smooth muscle activation on the right ventricular-vascular coupling during acute PH. PA flow, pressure, and diameter, right ventricular and aortic pressures were recorded in six anesthetized sheep. Acute PH was induced by phenylephrine (APH) and PA mechanical constriction (PPH). We calculated the PA buffering function, the incremental elastic modulus and pulmonary vascular compliance. Pulmonary vascular impedance and right ventricular hydraulic power were calculated through Fourier approach. We also quantified the magnitude and timing of the reflected wave. Right ventricular-vascular coupling was assessed by the energy transmission ratio. Pulmonary buffering function and vascular compliance increased (P<0.05) and arterial wall stiffness decreased (P<0.05) during APH with respect to PPH. Although total input resistance increased and reflected wave came back earlier during PH states (P<0.05), only PPH produced a rightward shift of the pulmonary impedance and a more prominent reflected wave. Accordingly, APH determined a minor increase of total hydraulic power with a smaller pulsatile to total power ratio and energy transmission ratio (P<0.05). In conclusion, isobaric PA vasoconstriction prevents the pulsatile hydraulic load to increase by preserving the PA buffering function and the reflected wave magnitude. Thus, vascular smooth muscle activation of the main PA improves the energy transfer from the right ventricle to the hypertensive pulmonary circulation, and this may play relevant role in the right ventricular adaptation to acute PH.

Adaptation, Physiological↗

PubMed2006

Cryopreservation procedure does not modify human carotid homografts mechanical properties: an isobaric and dynamic analysis.

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.

Carotid Arteries↗

PubMed2006

[Viscoelastic and functional similarities between native femoral arteries and fresh or cryopreserved arterial and venous homografts].

INTRODUCTION AND OBJECTIVES: It is not yet known whether cryopreservation enables vessels to retain their viscoelastic properties or whether cryopreserved homografts are biomechanically more like native arteries than currently used vascular prostheses. The study objectives were: a) to determine whether our cryopreservation methodology enables arterial and venous homografts to retain their viscoelastic and functional properties; and b) to assess similarities between patients' femoral arteries, homografts, and other vascular prostheses in common use. METHODS: The pressure and the diameter and parietal thickness of 15 muscular (femoral) arteries were measured in patients using tonometry and echography, both noninvasive techniques. In addition, the pressure in and diameter and parietal thickness of 15 fresh and 15 cryopreserved human muscular (femoral) artery segments, saphenous veins, and 15 expanded polytetrafluoroethylene (ePTFE) vascular prostheses were measured in vitro under hemodynamic conditions similar to those in patients. A Kelvin-Voigt model of the segment wall was used to derive elastic (Epd, mm Hg/mm) and viscous (Vpd, mm Hg x s/mm) pressure-diameter indices, the buffering function (Vpd/Epd), and the conduit function (1/Zc, where Zc is the characteristic impedance). The incremental Young modulus, the pressure-strain elastic modulus, and pulse wave velocity were also calculated. RESULTS: No difference was observed between either the viscoelastic or functional properties of fresh and cryopreserved homografts. Arterial homografts were the most similar to the patient's arteries. CONCLUSIONS: Cryopreservation enabled venous and arterial homografts to retain their viscoelastic and functional properties. Of all the grafts investigated, arterial homografts were most similar, both biomechanically and functionally, to the patient's femoral arteries.

Blood Vessels↗

PubMed2005

Femoral arteries energy dissipation and filtering function remain unchanged after cryopreservation procedure.

The aim was to evaluate our cryopreservation method effects on the mechanical properties and filtering function of human superficial femoral arteries (SFA). SFA segments from 10 multiorgan donors were divided into two groups: fresh, tested 24-48 h after harvesting, and cryopreserved/defrosted, tested after 1 month of cryopreservation. The cooling process was carried out in three steps: 2 degrees C/min until -40 degrees C; 5 degrees C/min until -90 degrees C and finally a rapid cooling by transferring the bag to vapour phase of liquid nitrogen (-142 degrees C). Thawing was made in two steps, a slow warming time by exposing the bag to 20 degrees C during 20 min, followed by a rapid warming by immersion in a 40 degrees C warm bath until defrost. In a circulation mock, arterial pressure [Pressure signal (P)] and diameter [Diameter (D)] were registered at similar stretch-frequency, P and flow levels. A compliance transfer function (D/P) was used for the on-line assessment of the arterial wall elastic (E), viscous (eta), and inertial (M) properties. To evaluate the arterial wall filter function, the arterial wall D/P frequency response was characterized, the cut-off frequency (fc) was quantified, and the viscous energy dissipation (Weta) was calculated. After cryopreservation, there were not significant changes in E, eta, M, Weta, and fc.

Adult↗

PubMed2005

[Regional differences in viscosity, elasticity and wall buffering function in systemic arteries: pulse wave analysis of the arterial pressure-diameter relationship].

INTRODUCTION AND OBJECTIVES: Regional variations in the incidence of vascular diseases have been related to regional differences in arterial viscoelasticity. The aim of this study was to characterize the differences in the elastic and viscous modulus and in wall buffering function between central and peripheral systemic arteries, through a time-series analysis of the pressure-diameter relationship. MATERIAL AND METHOD: Pressure and diameter were measured in seven arterial segments (carotid, brachiocephalic trunk, ascending aorta, proximal, middle and distal descending thoracic aorta, and femoral artery) from six sheep. Each segment was mounted on an in vitro mock circulatory system and perfused with Tyrode solution, with a pulse frequency of 1.8 Hz and systemic pressure levels. We used the Kelvin-Voigt model to calculate the pressure-diameter elastic (Epd, mmHg/mm) and viscous (Vpd, mmHg.s/mm) modulus, and to quantify the local wall buffering function (Vpd/Epd). We also calculated the incremental Young's and pressure-strain elastic modulus and pulse wave velocity for each segment. RESULTS: The elastic and viscous modulus increased from proximal to distal segments. The wall buffering function did not differ significantly between arteries. The lower rigidity of the central arteries compared to the distal ones may indicate that the systolic arterial compliance function is concentrated in the central arterial segments. On the other hand, the greater viscosity in the distal segments may indicate that viscous energy loss is concentrated in these segments. CONCLUSIONS: Arterial elasticity and viscosity can be interpreted as properties that are dependent on the region of the vessel, whereas wall buffering function can be considered region-independent.

Animals↗

PubMed2003

Improved pulmonary artery buffering function during phenylephrine-induced 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. 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.

Animals↗

PubMed2003

[Acute pulmonary hypertension: protective role of vascular smooth muscle activation].

AIM: 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. MATERIAL AND METHOD: 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. RESULTS: 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 (p < 0.05); 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. CONCLUSIONS: 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.

Acute Disease↗

PubMed2003

[The vascular smooth muscle of great arteries: local control site of arterial buffering function?].

INTRODUCTION AND OBJECTIVES: To characterize the viscoelastic properties of the aorta and pulmonary arteries and the effects of vascular smooth muscle activation on arterial buffering function. MATERIAL AND METHOD: 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. RESULTS: Viscoelasticity was higher in the aorta than in the pulmonary artery (p < 0.05), however, parietal buffering function was similar in both. Global buffering function was highest in the systemic circuit (p < 0.05). 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 (p < 0.05), while local and global buffering functions returned to baseline values. CONCLUSIONS: 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.

Animals↗