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Biomedical subjects

J Levenson

Publications and source records attributed to J Levenson.

At least 109 records · Page 6Linked to original sources
PubMed1992

Non-beta-adrenergic-mediated peripheral circulatory hyperkinesia in hyperthyroidism.

Systolic time intervals and brachial circulation, evaluated by pulsed Doppler in terms of arterial diameter, blood velocity and flow, and vascular resistance, were studied in 12 hyperthyroid patients and in 12 normal controls. In patients, arterial circulation was studied before and during mechanical exclusion of the hand, and hemodynamic measurements were repeated after beta-blocker treatment and after obtainment of euthyroid state. Compared with controls, patients had higher heart rate (P < 0.001), lower systolic time intervals (P < 0.05, P < 0.01), and higher blood velocity (P < 0.05). Beta blockade decreased heart rate (P < 0.05, P < 0.001) but did not change systolic time intervals and arterial circulation. Euthyroid state decreased heart rate (P < 0.01), preejection period (P < 0.01), and blood velocity (P < 0.01) and flow (P < 0.05). The decreases in velocity and flow before hand exclusion when euthyroid state was obtained were correlated with hyperthyroid values of velocity and flow respectively (r = 0.85, r = 0.90, P < 0.01, P < 0.001). Vascular resistance during hand exclusion was correlated negatively with serum T3 level during hyperthyroid and euthyroid states. Thus, thyroid hormones but not beta-adrenoreceptors participate in the peripheral hyperkinesia of hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed1992

Role of arterial compliance in the physiopharmacological approach to human hypertension.

Arterial compliance in humans is generally measured by modeling analysis of pulse tracing or of pulse wave propagation in the arterial tree. It is decreased in hypertension in part because elevation of blood pressure stiffens the arteries by stretching the rigid collagen fibres of their walls. Using a modeling evaluation of the compliance-pressure relationship in large arteries, it is possible to correct compliance from the mechanical effect (passive effect) due to pressure elevation. This makes it possible to show that, at the same pressure as in normal controls, hypertensive patients maintain decreased arterial compliance. This finding suggests that functional and/or structural changes other than pressure-mediated stretching of arteries (active effect) contribute toward reducing arterial compliance. Thus, the response of compliance to antihypertensive drugs must be studied by differentiating between passive and active effects. The diameter and compliance-pressure relationship in arteries allow differentiation of a passive arterial effect due to the pressure-lowering action of the drug, and an active pharmacological effect calculated at the same pressure before and after drug administration. Four drugs--ketanserin, urapidil, nitrendipine, and nicardipine (acute administration)--are given as examples. No active or passive compliance changes are observed with urapidil and ketanserin. In contrast, an active increase in compliance is observed in isobaric conditions with calcium antagonists, together with large-artery dilation due to a potent smooth muscle-relaxing effect. This active increase in compliance is potentiated by a passive increase due to the pressure-lowering effect that reduces the mechanical stretch exerted by blood pressure on arterial bioelastomers. Finally, an optimum increase in arterial compliance is achieved by drugs that vasodilate large arteries by smooth muscle relaxation and concomitantly decrease blood pressure. This may be of importance because low compliance has adverse effects on the cardiovascular system by contributing to the pathogenesis of systolic hypertension and left ventricular hypertrophy. Loss of arterial compliance may also be an early marker of atherosclerosis.

Antihypertensive Agents↗
PubMed1992

[Hypertension has no effect on coronary calcifications in asymptomatic patients with hypercholesterolemia].

Since calcium in coronary artery walls is considered as an indicator for atherosclerosis, we used ultrafast computed tomography to quantify it non invasively in 111 hypercholesterolemic men. They were selected at worksite by a cholesterol screening program, had total cholesterol (TC) above 5.2 (6.88 +/- 0.82, SD) mmol/l, were aged from 30 to 63 (46 +/- 5 years), had never been treated with lipid lowering or antihypertensive drug, and had no clinical coronary heart disease. Body mass index, blood pressure, smoking and other serum lipids as HDL cholesterol, triglyceride (TG) were evaluated. Calcium score of proximal coronary arteries was calculated on 30 contiguous 3 mm slices from areas and peak density of calcium lesions. The mean score was 30 +/- 69 and ranged from 0 to 440. A zero score was found in 39 subjects who differed from the 72 others only by TG levels (1.44 +/- 0.60 vs 1.85 +/- 0.80; p < 0.05). A multiple regression analysis showed that elevated calcium score was associated independently to age (F = 6.6; p < 0.05) and TG (F = 6; p < 0.05) but not to blood. Thus 65% of these asymptomatic subjects had a non-zero calcium score in coronary arteries. Elevated calcium score was influenced independently by age and triglyceride level, but not by other risk factors, such as blood pressure. This potential adverse effect of moderate triglyceride elevation on large coronary arteries merits attention in the assessment of the risk of coronary heart disease.

Adult↗
PubMed1992

[Increase of erythrocyte aggregation in hypertensive men with dyslipidemia].

We have already reported that erythrocyte aggregation (EA) is increased in hypertensive subjects. To study the influence of other risk factors in EA, we have measured aggregation index IA and disaggregation shear rate threshold (gamma c) by a laser technique and the biochemical parameters in 16 normotensive normocholesterolemic subjects (NT/NCT) and 45 hypertensive subjects where 17 were normocholesterolemic (HT/NCT), 18 were pure hypercholesterolemic (HT/HCTIIa) and 10 were hypercholesterolemic hypertriglyceridemic (HT/HCTIIb). The results show that IA and gamma c are more important in HT/NCT than NT/NCT patients and much more in patients with hypercholesterolemia and hypertriglyceridemia. The cumulative effects of hypertension and hyperlipidemia merit take into consideration in pathophysiology of cardiovascular complications and could help to new strategy therapeutic developments for treatment of these complications.

Adult↗
PubMed1991

Use of arterial compliance for evaluation of hypertension.

Arterial compliance describes a change in the volume of arteries following a change in blood pressure. The physical basis of the compliance concept and experimental procedures in animals both indicate that the relation between arterial compliance and blood pressure pattern is often unclear. Compliance is pressure-dependent because of the biphasic elastin and collagen composition of arteries and, hence, decreases when blood pressure increases. Compliance also determines the pulsatile amplitude of the pressure wave by regulating the buffering function of an artery's face to the cardiac pump and, accordingly, its reduction induces a selective increase in systolic level. The questions are whether these theoretical and experimental phenomena can be extrapolated to human hypertension and whether they can be assessed from indirect measurement of arterial compliance by means of a time-domain analysis of arterial pressure and flow waves via various models of the arterial tree. Whatever the method and site of measurement, arterial compliance was found to be decreased in different forms of hypertension. This low compliance can be considered to have a causal role in elderly patients with isolated systolic hypertension. In contrast, in patients with systolo-diastolic hypertension physiologic and pharmacologic arguments exist against the fact that low arterial compliance may be the pure consequence of mean blood pressure elevation. Moreover, it is suggested that aging acts in concurrence with pressure elevation to decrease arterial compliance, and that in certain hypertensive patients additional factors, perhaps atherosclerotic in nature, contribute to impair the elastic properties of arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗
PubMed1991

Assessment of elastin and collagen contribution to aortic elasticity in conscious dogs.

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.

Angiotensin II↗
PubMed1991

Mechanical pressure versus intrinsic effects of hypertension on large arteries in humans.

Brachial artery diameter and compliance were measured in 23 normotensive control subjects and 49 hypertensive patients. The results were compared in isobaric conditions by a modeling analysis extrapolating from the measured data a short segment of the pressure-diameter and pressure-compliance curves in the artery. A logarithmic diameter-pressure function was used as well as measurements of brachial artery blood pressure and lumen diameter (by pulsed Doppler), and of brachial-to-radial pulse wave velocity (by mechanography). The measured values of diameter and compliance in the hypertensive patients were 109% and 63%, respectively, of the control group values. By extrapolating the data via the model at the same pressure level in all subjects (the average level of mean blood pressure of the two groups), the isobaric values of diameter and compliance in the hypertensive patients were 107% and 81%, respectively, of the control group values. Overall, measured isobaric diameters and measured compliance correlated with systolic, diastolic, and mean blood pressure values (p less than 0.001), whereas isobaric compliance correlated only with systolic (p less than 0.05) and pulse (p less than 0.01) pressure values. Thus, the increased diameter and reduced compliance of the brachial artery observed in hypertensive humans cannot be attributed solely to the stretching effect of elevated blood pressure, but also to intrinsic alteration of the arterial walls. These could represent either adaptative structural or functional changes secondary to the chronic increase in arterial pressure, or primary abnormalities of the vessel wall.

Adolescent↗
PubMed1991

Paradoxically decreased aortic wall stiffness in response to vitamin D3-induced calcinosis. A biphasic analysis of segmental elastic properties in conscious dogs.

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.

Animals↗
PubMed1991

Hypercholesterolemia modulates the effects of nitrendipine on blood pressure and platelet function in essential hypertension.

Both marked hypercholesterolemia and severe hypertension have been reported to be associated with an enhanced sensitivity of blood platelets to activating agents. To investigate a possible mutual synergistic effect of moderate hypercholesterolemia and mild hypertension on platelet reactivity, we studied in 29 patients the response to aggregating agents, ADP and collagen, and the intracellular cyclic AMP content and cytosolic Ca2+ concentration that participate, respectively, as inhibitory and stimulatory mediators in platelet responses. When compared to age- and blood pressure-matched patients with normal or slightly elevated plasma cholesterol, the patients with total platelet cholesterol higher than 6.4 mM were characterized by a decreased response to collagen and ADP (14.5 +/- 3.0 vs. 23.8 +/- 2.0 a.u. and 17.7 +/- 4.5 vs. 26.9 +/- 2.7 a.u., respectively), a tendency to a reduced cAMP content both in the basal state and after phosphodiesterase inhibition by Ro-15 2041 (2.83 +/- 0.18 vs. 3.26 +/- 0.22 mumol/10(8) cells and 4.57 +/- 0.29 vs. 5.38 +/- 0.36 mumol/10(8) cells, respectively), and no change in cytosolic Ca2+ concentration (190 +/- 11 vs. 203 +/- 13 nM). After a chronic treatment with nitrendipine (20 mg/day for 6 months), blood pressure, platelet [Ca2+]i and cAMP content decreased in the patients with normal or moderately elevated hypercholesterolemia (p less than 0.001, less than 0.001, and less than 0.05, respectively), but these effects were attenuated or absent in the patients with higher hypercholesterolemia. Plasma lipids and the platelet-aggregating response to ADP and collagen were unchanged by this long-term nitrendipine treatment in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1991

Physiopharmacological approach to mechanical factors of hypertension in the atherosclerotic process.

Hypertension may influence the atherosclerotic process of large arteries via pressure and shear forces. The pressure force dilates and stiffens arteries because of the non-linear elastic behaviour of arterial walls. This partly explains the increased diameter and decreased compliance of the brachial artery in hypertensive subjects compared with normotensive controls. However, pressure lowering by antihypertensive drugs does not always reverse large artery alterations indicating that other mechanisms are involved. Reversal of low compliance obtained with certain antihypertensive drugs is generally concomitant with large artery vasodilation, suggesting that smooth muscle relaxation plays a major role in the compliance response to drugs. Atherosclerosis associated with hypertension also causes additional loss of compliance and creates a vicious circle of sclerosis development by accelerating the biophysical fatigue of bioelastomers. Hypertension may contribute to atherogenesis by means of wall shear stress which is the frictional force exerted by the circulating blood column on the intima of arteries. Since it is likely that atherosis lesions may develop preferentially in low shear conditions, hypertension may promote the haemodynamic conditions of atherogenesis at the blood-wall interface. The response of wall shear to antihypertensive treatment is not unequivocal. For example, the beta-blocker, atenolol, does not change shear whereas carteolol increases shear rate and stress and these effects are closely related to change in platelet-free calcium concentration. This finding is consistent with the effect of shear forces on cell permeability to calcium demonstrated in vitro and points to the crucial role of wall shear as a biophysical signal capable of modifying the endothelial structure and function of arteries.

Antihypertensive Agents↗
PubMed1991

[Intrinsic (isobaric) effect of essential hypertension on visco-elastic properties of the brachial artery].

The purpose of this study was to estimate the effect of hypertension on the visco-elastic properties of the brachial artery in man. Seventy-five subjects including 23 with normal blood pressure (group N, PN = 95 +/- 7 mmHg, P designates the arterial mean pressure, P = DBP + (SBP-DBP)/3) and 52 with essential hypertension (group H, PH = 122 +/- 12 mmHg) participated to this study. We measured the diameter of the brachial artery (D) by the pulsed Doppler method, the brachial-radial pulse wave velocity (PWV) by the mecanographic method, and calculated the arterial compliance (C) by the Bramwell-Hill formula. A nonlinear model was used to calculate compliance and pression at any given pressure, in particular at PN or PH. We obtained the following results: [table; see text] Passive (pressure-induced) effect was obtained by comparing D(PH) to D(PN) and C(PH) to C(PN). Isobaric effect of hypertension was estimated by comparing D(PH) and C(PN) between the N and H groups. We concluded that hypertension actually induces a decrease in compliance. However, arterial diameter is increased in hypertension. The increase in diameter appears as a compensatory effect, without which the reduction in compliance would be more nocive to the circulatory system.

Adult↗
PubMed1991

[Increase of erythrocyte disaggregation shear rate in arterial hypertension].

Aggregation index and critical disaggregation shear rate (which represent the minimum shear rate necessary to break up the aggregates) have been measured for 21 hypertensive and 17 normotensive subjects by a laser technique (erythro-aggregameter SEFAM). A simultaneous measurement of blood viscosity by a Couette viscometer with coaxial cylinders at different shear rate allowed the calculation of critical disaggregation shear stress by the product of critical disaggregation shear rate and blood viscosity. The comparison of the results of normotensive and hypertensive subjects showed a higher aggregation index (22%, p less than 0.0001), critical disaggregation shear rate (19%, p less than 0.002) and critical disaggregation shear stress (29%, p less than 0.004) in hypertensive patients. These alterations might play an important role on development of cardiovascular complication in hypertensive subjects.

Adult↗
PubMed1991

[Comparison of isobaric effects of hypertension and diabetes mellitus on geometric and elastic properties of human arteries].

Hypertensive and diabetic mellitus diseases are known to increase stiffness of the arterial wall. However these alterations probably involve different mechanisms. To this end, we compared the effect of hypertension and diabetes on large artery caliber and elasticity at real pressure conditions and at the same level of pressure. Nine poorly controlled non insulino-dependent diabetic men without hypertension and 9 non-diabetic essential hypertensive men underwent measures of lumen diameter (pulsed Doppler) and segmental compliance (Bramwell and Hill formula; pulse wave velocity) at the brachial artery. Isobaric diameter and compliance were deduced from a non linear model, comparing diameter and pressure on one part, and compliance and pressure on the other. Pulse wave velocity was similarly increased in both diseases (11.5 +/- 1 vs 12.8 +/- 1 m/s; NS; respectively in diabetes and hypertension). Both measured and isobaric diameters were smaller in diabetic patients (4.05 +/- 0.2 vs 5.03 +/- 0.2 mm, p less than 0.1% for the measured diameters respectively in diabetes and hypertension and 4.06 +/- 0.2 vs 5.01 +/- 0.2 mm, p less than 1% for isobaric diameters). The measured and isobaric compliances were not significantly different (2.38 +/- 0.4 vs 2.08 +/- 0.2 cm/mmHg10(-4), NS, for the measured compliance respectively in diabetes and hypertension; 2.28 +/- 0.4 vs 2.4 +/- 0.2, NS for the isobaric compliance). After correction of the effect of mechanical arterial stretch induced by the different blood pressure level of the two groups, significant reduction of diameter in diabetic subjects persisted and isobaric and measured compliances remained unchanged between groups.

Adult↗
PubMed1991

Risk factors and early extracoronary atherosclerotic plaques detected by three-site ultrasound imaging in hypercholesterolemic men. Prévention Cardio-vasculaire en Médecine du Travail METRA Group.

Ultrasonic detection of atherosclerotic plaque of carotid abdominal aortic and femoral arteries and evaluation of risk factors were performed in 208 hypercholesterolemic men without cardiovascular disease. Twenty-six percent of them had no plaque. Plaque at the carotid, aortic, and femoral sites was found in 37%, 48%, and 53% of subjects, respectively. Plaque was associated (1) in carotid arteries with increased total and low-density lipoprotein cholesterol; (2) in the aorta with increased age, pressure, glycemia, and smoking; and (3) in femoral arteries with increased age, systolic pressure, low-density lipoprotein cholesterol, and smoking. Multiple regression analysis showed correlations between carotid plaque and low-density lipoprotein cholesterol; aortic plaque and age, smoking, glycemia, and pressure; femoral plaque and age, smoking, and pressure. This suggests that multiple risk factors influence lesions, and risk profile differs according to atherosis site.

Adult↗
PubMed1990

Mechanical factors in large artery disease and antihypertensive drugs.

Hypertension may induce early alterations in large arteries by 2 mechanical stresses: one related to intravascular pressure, the other to blood flow dynamics. Distending pressure force acts in a circumferential direction, inducing decreased arterial distensibility. Arterial distensibility can be evaluated in humans by measurement of arterial compliance and pulse-wave velocity. It is well established that in chronic hypertension age and elevated pressure act together to increase arterial rigidity. Blood flow dynamics induce frictional forces in the endothelial surfaces of arteries. These forces, expressed by shear stress, are proportional to the viscosity of the blood and to the velocity gradient at the arterial wall. Measurement of blood viscosity and evaluation of velocity profile in the brachial arteries of hypertensive subjects have shown a reduction in wall shear rate and stress despite the elevation in blood viscosity. Several studies have shown that drug therapy that successfully reduces blood pressure does not necessarily improve arterial compliance. In contrast, few data are available on the effects of antihypertensive medication on arterial wall shear in humans. Arterial compliance and wall shear stress are 2 main therapeutic targets of potential importance in the physiopharmacologic approach to the effects of hypertension on atherogenesis.

Antihypertensive Agents↗