Showing papers by "Stéphane Laurent published in 1997"

Increased Stiffness of Radial Artery Wall Material in End-Stage Renal Disease

Abstract: The incremental elastic modulus (Einc), which is the slope of the relationship between stress and strain of arteries, is a marker of vascular wall material stiffness. Isobaric Einc is reduced at the site of the radial artery in patients with essential hypertension and increased at the site of the common carotid artery in subjects with end-stage renal disease (ESRD). Whether the changes in Einc are influenced by the topography of the vessels, the composition of the arterial wall, and/or by the presence of ESRD is largely ignored. Radial artery Einc was measured in 19 patients with ESRD and compared with the Einc of 89 subjects with essential hypertension and 20 normotensive control subjects. Transcutaneous measurements of radial artery internal diameter and wall thickness (echo-tracking device) and digital pulse pressure (Finapres) were allowed to calculate Einc under operational (ie, at the mean arterial pressure of each group) and isobaric (100 mm Hg) conditions, as well as for a given wall stress. Internal diameter and pulsatile changes in diameter were identical in the three groups. Wall thickness and mean blood pressure were significantly elevated in subjects with hypertension but not in ESRD patients. Circumferential wall stress was identical in the three groups. For the same operational wall stress, and therefore at the operational mean arterial pressure of each group, Einc (kPa x 10[3]) was increased in patients with ESRD (5.53+/-4.0 versus 3.3+/-2.4 in control subjects; P<.05) and normal in subjects with essential hypertension (3.87+/-4.0). Under isobaric conditions, Einc was also significantly lower in subjects with hypertension and elevated in patients with ESRD. Thus, at the site of a medium-sized muscular artery constantly devoid of atherosclerosis, the stiffness of wall material is increased in patients with ESRD. The demonstrated alterations of the arterial wall are independent of the level of blood pressure and tensile stress and should be related to the status ESRD.

Large artery stiffness in hypertension.

Abstract: EFFECTS OF HYPERTENSION ON LARGE ARTERIES: The mechanical properties of large arteries make a major contribution to cardiovascular haemodynamics through the buffering of stroke volume and by propagation of the pressure pulse. A sustained increase in blood pressure often leads to stiffness of the large arteries, especially when other risk factors are present. The increased stiffness, in turn, aggravates hypertension by increasing systolic blood pressure and can induce cardiac hypertrophy and arterial lesions. Epidemiological studies strongly suggest that subjects with stiffer arteries have a high pulse pressure, and that stiffening of large arteries is associated with excess morbidity and mortality independently of other cardiovascular risk factors. ENVIRONMENTAL AND GENETIC FACTORS: Apart from high blood pressure and ageing, various environmental and genetic factors that influence the composition of the extracellular matrix of the arterial wall can increase arterial stiffness. Clinical studies suggest that the presence of some genotypes may be a particularly important risk marker for arterial stiffness, and may modulate the effects of hypertension, ageing and lipids on large arteries. EFFECTS OF ANTIHYPERTENSIVE DRUGS: The development of accurate, non-invasive methods has now made it possible to detect alterations of the large arteries. Among antihypertensive drugs, angiotensin converting enzyme inhibitors and calcium channel blockers have proved to be highly effective in improving large artery compliance, and have shown no adverse effects on metabolic factors that can alter arterial structure and function such as lipids, plasma glucose and insulin tolerance. Therefore these drugs may be particularly suitable for treating patients with increased arterial stiffness. Finally, a determination of genotypes may be helpful in the future in choosing antihypertensive therapy.

In Vivo/In Vitro Comparison of Rat Abdominal Aorta Wall Viscosity Influence of Endothelial Function

Abstract: Arterial wall viscosity (AWV) is a potential source of energy dissipation in circulation. That arteries, which are known to be markedly viscous in vitro, have lower viscosity in vivo has been suggested but not demonstrated under similar pressure conditions. Endothelium, which may modulate AWV through smooth muscle tone, could contribute to the low level of viscosity in vivo. Our objectives were first to compare AWV of the rat abdominal aorta, in vivo and in vitro, with similar pulse-pressure waves, and second, to determine whether endothelial function influences AWV in vivo and in vitro. The diameter of the abdominal aorta and distending pressure were measured in vivo and in vitro with a high-resolution echotracking system and a micromanometer, respectively. AWV was calculated as the area of the pressure-volume curve hysteresis. After in vivo examination, the arterial segments were isolated in vitro and submitted to resynthesized pressure waves identical to those recorded in vivo. Deendothelializ...

Mechanical Stress of the Carotid Artery at the Early Phase of Spontaneous Hypertension in Rats

Abstract: Common carotid artery (CCA) hypertrophy has long been recognized in the neonatal period of development in spontaneously hypertensive rats (SHR), but the mean circumferential and shear stresses acting on the arterial wall have never been investigated in vivo. We investigated intra-arterial blood pressure in conscious rats, CCA diameter (echotracking techniques), blood flow velocity (pulsed Doppler), wall thickness (histomorphometry), and ganglionic blockade (hexamethonium) in Wistar rats and SHR at 5 and 12 weeks of age. During this interval, weight gain was identical in the strains, whereas the increase in wall thickness and blood pressure was greater in SHR. CCA diameter was identical at week 5 and increased similarly at week 12 in both strains. During ganglionic blockade, a larger diameter was observed in SHR at week 5 for the same BP level, whereas equivalent values were observed at week 12. Blood flow velocity decreased with age but to a significantly greater extent in SHR. Mean circumferential stress and shear stress index were identical in both strains at week 12. However, from weeks 5 to 12, mean circumferential stress increased with age similarly in both strains, whereas the age-related decrease in mean shear stress index was much greater in SHR than Wistar rats. Thus, despite a higher blood pressure, SHR exhibit the same carotid diameter as Wistar rats during early development. Because the kinetics of shear stress are different in both strains, altered flow-dilatation mechanisms, and possibly resulting endothelial dysfunction, may be involved in the diameter changes.

Effects of clonidine and flesinoxan on blood pressure variability in conscious spontaneously hypertensive rats.

Abstract: Summary: The effects of two centrally acting antihypertensive agents, clonidine (0.1 mg/kg/day s.c.) and flesinoxan (1 mg/kg/day s.c.), on short-term blood pressure variability (BPV) were investigated in conscious spontaneously hypertensive rats (SHRs). The drugs were infused subcutaneously during 24 h and 4 weeks by osmotic minipumps. BPV was characterized by spectral analysis. In conscious SHRs, clonidine significantly and preferentially reduced the low frequency (LF; 0.25-0.75 Hz) oscillations of mean arterial pressure (MAP) in short-term (24 h) and long-term (4 weeks) treatments but significantly decreased MAP level only in short-term treatments. In contrast, flesinoxan significantly reduced MAP level whatever the duration of infusion but decreased LF-MAP only in short-term treatments. These results show that centrally mediated inhibition of sympathetic tone by stimulation of either α2-adrenoceptors or 5-HT1A (serotonin) receptors can reduce BPV. This effect is independent of the modifications in BP level. The effects of the drugs on baroreceptors may also contribute to the decrease in BPV. The dual properties of clonidine (α2-adrenoceptors and imidazoline receptors) may account for its differential effects on BP level and BPV.

The wall to lumen ratio of the radial artery in patients with Raynaud's phenomenon.

Abstract: The pathophysiology of Raynaud’s phenomenon (RP) remains an enigma. Whatever theories proposed, the final event leading to the clinical symptoms is the occlusion of digital vessels. However, the possi

Interactions cellule/matrice et propriétés élastiques des gros troncs artériels

Abstract: Les proprietes mecaniques des parois arterielles dependent des cellules musculaires lisses, et des contenus en collagene et en elastine de la media. L'organisation spatiale de ces differents elements est en partie reglee par les interactions entre les proteines d'adherence de la matrice extracellulaire et les integrines a la surface des cellules. La transmission des signaux mecaniques prend son origine au niveau des plaques denses ou hemi-desmosomes, composees de proteines du cytosquelette liees aux proteines d'adherence de la matrice extracellulaire par les integrines. Chez le rat spontanement hypertendu la fibronectine en exces semble contribuer a proteger la paroi arterielle contre les degats mecaniques. Au cours de l'atherome, l'organisation initiale de la plaque s'accompagne de surproduction de la matrice extracellulaire, alors qu'aux stades ulterieurs la priorite revient a l'adherence par l'intermediaire des integrines, prevenant la rupture de la plaque. Le role des integrines dans le fonctionnement de la paroi arterielle semble majeur mais reste a ce jour encore mal connu.

Physiopathologie du remodelage artériel dans l'hypertension artérielle

Abstract: Il existe schematiquement deux types de modifications arterielles en reponse a l'hypertension, capables toutes deux de diminuer la lumiere arterielle : l'hypertrophie, avec augmentation du volume de la paroi, et le remodelage, ou le volume parietal n'est pas modifie. Ces dernieres annees, le remodelage arteriel s'est impose comme un concept cle de la physiopathologie de l'hypertension arterielle, source de multiples applications pharmacologiques. La meilleure connaissance des modifications ultra-structurales et geometriques dans les arteres de gros, moyen et petit calibre (arteres resistives) a modifie leur approche therapeutique en offrant de nouvelles cibles pharmacologiques : facteurs de croissance et recepteurs specifiques divers des cellules musculaires lisses et endotheliales, recepteurs et enzymes de la matrice extracellulaire.