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Biomedical subjects

J Levenson

Publications and source records attributed to J Levenson.

At least 145 records · Page 8Linked to original sources

[Non invasive evaluation of endothelial shearing phenomena in human arteries. Application to essential hypertension].

Pulsatile wall shear conditions close to the brachial artery were evaluated in 11 normotensive and in 19 hypertensive patients of similar age by determining arterial diameter and centerline blood velocity with a pulsed Doppler and blood viscosity at 96 sec-1 with a coaxial cylinder viscometer. A Womersley model of intraluminal distribution of blood velocities enabled to determine from unsteadiness parameter alpha of Womersley, arterial diameter and maximal minimal and pulse (maximal-minimal) values of centerline velocity, the maximal minimal and pulse shear rate and shear stress (product between shear rate and viscosity) close to the endothelium. Compared to normotensives hypertenvises had higher arterial diameter (p less than 0.001), lower maximal minimal and pulse centerline velocities (p less than 0.001, p less than 0.01, p less than 0.001) higher blood viscosity (p less than 0.001), lower maximal, minimal and pulse wall shear rate (p less than 0.001, p less than 0.05, p less than 0.001) and lower maximal minimal and pulse shear stress (p less than 0.01). In the overall normotensive and hypertensive group, mean blood pressure negatively correlated to maximal minimal and pulse shear rates (r = -0.65; r = -0.45, r = -0.63) and to maximal, minimal and pulse shear stress (r = -0.46; r = -0.37, r = -0.48). Thus, hypertension is associated with a reduction of oscillating shear conditions in the viscosity of the brachial artery wall which might in long term influence structural and/or functional response to the endothelium.

Adult↗

[Essential hypertension and platelet cytosolic concentrations of H(+) and Ca2(+)].

Essential hypertension is associated with various cell abnormalities, including alterations in the metabolism of intracellular messengers, such as cytosolic free Ca2+ and cyclic AMP or IP3. Intracellular pH is implicated in the regulation of number vital functions, including cell metabolism, division and response to various stimuli. We have measured cytosolic H+ concentration ([H+]i) in human platelets and investigated a possible relationship with free Ca2+ concentrations ([Ca2+]i) in hypertensive patients. [H+]i was determined with the pH sensitive fluorescent probe BCECF in platelets from 15 normotensive subjects and 15 patients with mild to moderate essential hypertension, free from medication, il any, for at least two weeks. Donor characteristics are indicated in the table. (table; see text) [H+] cytosolic from hypertensive patients was significantly lowered by 21 p. 100 compared to normotensive values (table). Cytosolic free Ca2+ concentrations, measured with the Ca2+ fluorescent probe Fura2, were significantly increased by 19 p. 100 in platelets from hypertensive patients when compared to those of normotensive donors. Taken all together, [H+]i and [Ca2+]i varied inversely (r = -0.421, p = 0.02) in these thirty donors and tends to be correlated in the essential hypertensive patients (r = 0.490, p = 0.06). This correlation remained significant at constant age systolic and diastolic blood pressures. The simultaneous rise in [H+]i and [Ca2+]i in platelets from essential hypertensive patients are compatible with their observed enhanced sensitivity to several aggregating agents. This alkalinisation, if present in the vascular smooth muscle cells, may also reflect facilitated cell proliferation and increased sensitivity to stimulating agents, two parameters implicated in the rise of arterial blood pressure.

Adult↗

[Blood viscosity is a chronic adjustment factor of arterial vasodilatation in humans].

Arteriolar geometry and blood viscosity, the two main factors determining vascular resistance were studied in 44 normotensive subjects and 106 hypertensive patients at the brachial circulation level. Vascular resistance was calculated as the ratio between mean blood pressure and mean arterial flow determined by pulsed Doppler. Blood viscosity at 240 sec-1 was measured with a coaxial cylinder viscometer: Compared to controls, hypertensive patients had higher vascular resistance (161 + 8 vs 124 + 9 mmHg.ml-1.sec, P less than 0.05) and higher viscosity (4.75 + 0.05 vs 4.50 + 0.07 mPasec, P less than 0.01). Vascular resistance was negatively correlated to blood viscosity both in control (r = 0.48; P less than 0.001) and in hypertensive (r - 0.39, P less than 0.001) groups. Arteriolar equivalent radius (a) calculated from Poiseuille's equation from the relation a = (8 mu/pi R) 1/4 was positively correlated to viscosity in the two regressions were statistically different (P less than 0.001) indicating that at higher viscosity levels, arteriolar equivalent radius had lesser increase in normotensive than in hypertensive groups. Thus chronic increase in blood viscosity is accompanied by a small vessels vasodilatory phenomenon which seems less efficient in normotensive than in hypertensive subjects and might contribute in part to the mechanisms of vascular resistance elevation observed in hypertension.

Adult↗

[Paradoxal diminution of resistance of the large arteries in human essential hypertension].

Segmental pressure drop and longitudinal resistance of brachial artery were evaluated in 11 normotensive (NT) and 19 hypertensive (HT) subjects of similar age by measuring arterial diameter (D), blood velocity (V) and flow (Q) with pulsed Doppler and blood viscosity (mu) at 96 sec-1 with a coaxial cylinder viscometer. Mean pressure drop (delta P) per unit of length of artery was calculated according to the relation delta P = 4 tau/D, where tau is the mean wall shear stress evaluated on the basis of a Poiseuille velocity profile by the formula: r = vV/D. Brachial artery resistance per unit of length was deduced as the (delta P/Q) ratio. (table; see text) In the overall normotensive and hypertensive group, (n = 30), pressure drop (delta P) was negatively correlated with mean blood pressure (r = -0.55, P less than 0.01). Despite increased viscosity hypertensive patients have a decreased resistance of large arteries whose mechanisms include a reduction in shear stress close to the endothelium and a dilation of the conduit artery; these two abnormalities contribute to decrease the viscous force of the circulating blood column against the arterial wall.

Adult↗

[Visco-elastic characteristics of the aorta in conscious dogs in a model of experimental calcinosis].

Effects of experimental calcinosis induced by daily overdose of 500.000 IU Vit D3 during 10 days were studied in 6 mongrel conscious dogs chronically instrumented with intra-aortic Konigsberg microtransducer and two ultrasonic piezo-electric crystals diametrically opposed in the adventitia of the descending thoracic aorta. Simultaneous recording of instantaneous aortic pressure and diameter waves in basal state and during transient acute hypertension induced by intravenous angiotensin bolus (0.1 microgram/kg) allowed to obtain the pressure (y) diameter (x) relationship of the aorta according to an exponential regression: P = expo (beta D + A), with a highly significant correlation coefficient in all animals (r greater than 0.99). (table; see text) Anatomopathological studies of aortas revealed abnormal calcium deposition, ruptures of elastic fibers and disorganization of collagen. Thus, a striking decrease in aortic rigidity is observed after calcinosis in relation with structural changes of elastic materials and responsible in part for a reduction in pulsatile pressure; moreover this unexpected phenomena might represent an initiative process of development of aortic aneurysms.

Animals↗

Unrelated responses of brachial artery hemodynamics and renin-angiotensin system to acute converting enzyme inhibition by enalaprilat in essential hypertension.

The simultaneous acute effects of converting enzyme inhibition by intravenous enalaprilat on the circulating renin-angiotensin system and on the brachial artery were studied in 12 hypertensive patients by a double-blind comparison with saline effects in 14 hypertensive patients. The brachial artery was investigated in terms of arterial section (measured by pulsed Doppler technique) and wall rigidity (assessed by pulse wave velocity). Arterial and biochemical parameters were measured in baseline before injection and at 20 to 40 minutes (t1) and 80 to 100 minutes (t2) after saline and drug injections. Compared with the saline vehicle, enalaprilat significantly decreased angiotensin enzyme converting activity (p less than 0.001), increased plasma renin activity (p less than 0.01) and decreased plasma aldosterone concentrations (p less than 0.01). The drug reduced blood pressure (p less than 0.01) and increased the brachial artery section (p less than 0.01), but did not change pulse wave velocity. In the enalaprilat group, significant postinjection relations were observed between: (1) enalaprilat concentration and plasma angiotensin converting enzyme activity (r = -0.72, p less than 0.001); (2) plasma renin activity and mean blood pressure (r = -0.46, p less than 0.02); (3) plasma enalaprilat concentration and pulse wave velocity (r = -0.50, p less than 0.01) and (4) pulse wave velocity and brachial artery section (r = 0.42, p less than 0.05). Thus, the brachial artery effects of enalaprilat were not directly related to the blockade of the renin-angiotensin system in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Brachial artery hemodynamic response to acute converting enzyme inhibition by enalaprilat in essential hypertension.

To assess the vascular involvement of renin-angiotensin system inhibition in human hypertension, acute effects of intravenous enalaprilat on brachial artery diameter, blood flow, and blood velocity were investigated in hypertensive patients by pulsed Doppler technique and compared with effects of saline vehicle. Compared with saline vehicle, enalaprilat reduced blood pressure (P less than 0.001) and increased brachial arterial diameter (P less than 0.01) and brachial blood flow (P less than 0.01). Enalaprilat effect on arterial pulse pressure was dependent on preinjection pulse pressure (r = -0.76; P less than 0.001), but its effect on mean blood pressure was not dependent on preinjection mean blood pressure. On the other hand, enalaprilat effect on arterial blood flow was negatively correlated with preinjection blood pressure (r = -0.64; P less than 0.02). The findings point to different responses of large and small arteries to intravenous enalaprilat.

Angiotensin-Converting Enzyme Inhibitors↗

Combined effects of gender and hypertension on the geometric design of large arteries. Sexual differences in normal and hypertensive forearm arteries.

The effects of sex, hypertension, morphologic status, and heart rate were assessed on the large arteries of 46 normotensive subjects (23 men and 23 women) and 50 hypertensive patients (25 men and 25 women) by means of pulsed Doppler determination of diameter and blood velocity of the brachial artery. Compared to men, women had lower height, weight, and forearm volume (P less than 0.001), higher heart rate (P less than 0.001), and lower brachial artery diameter (P less than 0.001) both in the normotensive and hypertensive groups. Compared to normotensives, hypertensives of the same sex showed an increase in brachial artery diameter, only significant in men (P less than 0.001), and an increase in heart rate, only significant in women (P less than 0.001). The multiple regression analysis of brachial artery diameter showed significant coefficients for sex and hypertension (P less than 0.001), and for age and heart rate (P less than 0.05); the multiple regression analysis of blood velocity showed that only the coefficient of hypertension was significant (P less than 0.05). The study of first-order interactions between the independent variables revealed that effect of sex on arterial diameter did not depend on the other variables. In contrast the effects of age and heart rate were influenced by the presence or the absence of hypertension, and arterial caliber was positively related to age in normotensive subjects (P less than 0.05) but not in hypertensive patients, and negatively related to heart rate in hypertensive patients (P less than 0.001) but not in normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Opposite effects of hypertension and smoking on large artery wall shear conditions.

Wall shear phenomena were studied in the brachial artery in non-smoking and smoking normotensive and hypertensive subjects of similar age. Pulsed Doppler investigation revealed brachial artery diameter, and mean and systolic blood velocities (at the centerline of the vessel). A Poiseuillean blood velocity distribution was used to determine the wall shear rate and stress from velocity, diameter and viscosity. This was expressed in terms of mean and systolic values. Although hypertension and smoking both increased blood viscosity, hypertension reduced mean and systolic shear rates and stresses in non-smokers but not in smokers, and smoking increased mean and systolic shear rates and stresses in hypertensives but not in normotensives. Thus, the decreasing shear effect of hypertension was blunted by smoking, while the increasing shear effect of smoking was elicited by hypertension, suggesting an interaction of these factors on wall shear conditions.

Arteries↗

Aortic pulsatile pressure and diameter response to intravenous perfusions of angiotensin, norepinephrine, and epinephrine in conscious dogs.

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.

Angiotensin II↗

Constricting and stiffening action of atropine on aortic response to angiotensin in dogs.

The elasticity of the thoracic aorta was studied in nine dogs instrumented with a pressure microtransducer and two ultrasonic crystals diametrically fixed in the adventitia. Systolic and diastolic changes in pressure and diameter were used to calculate Peterson and incremental elastic moduli. Acute hypertension was induced by infusions of angiotensin performed 1) during the control period, 2) after propranolol (1.5 mg/kg), 3) after atropine (0.2 mg/kg), and 4) after propranolol plus atropine. Absolute and percent variations of mean diameter were correlated to pressure in the control period and after autonomic blockade (p less than 0.01). The slopes of these correlations were not different between propranolol and control groups, but were lower with atropine (p less than 0.01) and with atropine plus propranolol (p less than 0.001) than in the control period. Correlations were also found between Peterson and incremental elastic moduli and mean pressure in the control period and after blockade (p less than 0.001). No differences of slopes existed between propranolol and control groups, but the slope of the correlation relative to the incremental elastic modulus was higher with atropine than in the control period (p less than 0.05), and the slopes of the correlations relative to the Peterson and the incremental elastic moduli were respectively higher with atropine plus propranolol than in the control period (p less than 0.05, p less than 0.05). Thus, atropine decreased the distention and increased the stiffness of the aorta in response to acute angiotensin-mediated hypertension.

Angiotensin II↗

Heterogeneity of response of peripheral arteries to antihypertensive drugs in essential hypertension. Basic effects and functional consequences.

The vascular impact of different antihypertensive drugs was assessed in patients with mild to moderate essential hypertension by the use of the forearm circulation as a simple model to characterise the geometrical and distensible properties of the arterial system. The acute and chronic responses of the forearm arteries, expressed in terms of geometry (vasodilatation or vasoconstriction) and distensibility (arterial compliance, pulse-wave velocity), were not solely dependent on blood pressure levels. For similar blood pressure decreases, the dilatation of the forearm resistive vessels was associated either with an increase (calcium antagonists, angiotensin-converting enzyme inhibitors) or with a reduction (hydralazine-like drugs) or with no change (alpha- and beta-blocking drugs) in the calibre of the large forearm vessel. These non-homogeneous geometrical responses to antihypertensive drugs had important haemodynamic effects on the conduit, the buffering and the baroreflex functions of the arterial tree.

Antihypertensive Agents↗

[Constrictive and stiffening effects of parasympathetic blockade on the pressure response of the aorta to angiotensin in the conscious dog ].

The elastic response of the thoracic aorta to increasing steps of angiotensin was studied in chronic instrumented conscious dogs with and without parasympathetic blockade by atropine. A pressure microtransducer and two ultrasonic crystals diametrically opposed and fixed in the adventitia enabled to determine the mean and systolic-diastolic changes of pressure (P) and diameter (D). By computing these measurements two representative indexes of dynamic elastic modulus in vivo were calculated; the elastic modulus of Peterson (Ep) Ep = delta P/D.D and the incremental elastic modulus (Ei) Ei = 0.75 EP/gamma, gamma being the ratio of the thickness to the external radius. A positive correlation (p less than 0.01) was obtained between pressure and diameter variations in the presence or absence of atropine but the slope of these relationship were lower with atropine than in controls. The slope of the positive correlations observed between Peterson and incremental elastic modulus and the increase in mean arterial pressure in response to angiotensin (p less than 0.01) was higher in the presence of atropine (p less than 0.05). These observations indicate that in response to angiotensin mediated high blood pressure, the cholinergic blockade of muscarinic receptors with atropine induce a contraction and increasing rigidity of the aorta.

Angiotensin II↗

[Shearing anomalies of the arterial endothelium in essential arterial hypertension].

Brachial artery wall shear rate and stress were studied in 20 untreated hypertensive patients and 11 normotensive controls of similar age. A pulsed Doppler velocimeter enabled to determine the internal diameter, the mean cross-sectional blood velocity and the systolic centerline blood velocity of the brachial artery. A coaxial cylinder viscosimeter provided blood viscosity at a shear rate of 96 s-1. A Poiseuille model of arterial flow was used for evaluating wall shear rate from the ratio between blood velocity and arterial diameter and wall shear stress from the product between shear rate and blood viscosity. Shear rate and stress were expressed in terms of systolic and mean values by using respectively systolic centerline and mean cross-sectional blood velocities. Comparatively to normal controls, hypertensive patients had higher blood viscosity (4.80 +/- 0.08 vs 4.28 +/- 0.09 cpoise, p less than 0.001) lower systolic wall shear rate (303 +/- 18 vs 413 +/- 20 s-1, p less than 0.001), lower mean wall shear rate (70 +/- 6 vs 109 +/- 16 s-1, p less than 0.01) and lower systolic wall shear stress (13.86 +/- 0.81 vs 17.02 +/- 1.26, p less than 0.001) but mean wall shear stress was not statistically different between patients and controls. Such wall shear abnormalities are described for the first time in large artery of hypertensive patients and merit attention because of the experimental critical role of low shear conditions on the atherogenic process.

Adult↗

[Effect of age on brachial and carotid circulation in human arterial hypertension].

Right brachial artery and common carotid artery haemodynamic parameters were studied using pulsed Doppler velocimetry enabling non invasive measurements of their internal diameters and blood velocities in 74 untreated essential hypertensive patients subdivided in two groups of younger than (33 patients) and older than 45 years (41 patients). There were no significant differences in the haemodynamic parameters of brachial artery (i.e. diameter and blood velocity) between the two groups of patients. In the patients older than 45, there were no changes in the diameter of common carotid artery, but there was a decrease in carotid artery blood velocity as compared with patients younger than 45 (p less than 0.001). In the patients younger than 45, there were no correlations between the haemodynamic parameters of both circulations; in contrast, in patient older than 45 significant relationship were found between the common carotid artery diameter and the brachial artery diameter (r = 0.45, p less than 0.01) and between the blood velocity in the common carotid artery and in the brachial artery (r = 0.55, p less than 0.001). Thus, in these hypertensive patients, brachial artery circulation was not affected by age; but age older than 45 was associated with a decrease in common carotid blood flow, with no change in common carotid artery diameter. However, the existence of strong correlations between brachial and carotid artery diameters and blood velocities in patients older than 45, suggests that age might interfere, in hypertensive patients, with the specific regulatory adjustments of the brachial and carotid circulations.

Adult↗

Heterogeneity of the atherosclerotic process in systemic hypertension poorly controlled by drug treatment.

A cross-sectional study of 85 patients with poorly controlled treated hypertension was performed to detect, by means of aortic pulse wave velocity measurement and ultrasonic examinations, subclinical alterations of arteries. Pulse wave velocity was related to the product of age and diastolic blood pressure (BP) according to a nomogram obtained from normotensive subjects, and was found inside the nomogram in 37 patients (group I) and outside in 48 (group II). Group II had higher systolic and pulse BP (p less than 0.01), lower diastolic BP (p less than 0.01), higher proportion of cigarette smokers (p less than 0.05) and higher blood glucose levels (p less than 0.02) than group I. In group II a positive correlation existed between blood glucose and pulse wave velocity (p less than 0.01). Group II had a higher frequency of carotid artery stenosis (p less than 0.05) and a trend toward increased frequency of aortic and lower limb atherosclerotic lesions. The results indicate a heterogeneous pattern of arterial alterations in which systolic BP, cigarette smoking and blood glucose level are implicated.

Age Factors↗