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Biomedical subjects

A Tedgui

Publications and source records attributed to A Tedgui.

At least 109 records · Page 6Linked to original sources
PubMed1993

Protection from atherosclerosis in vein grafts by a rigid external support.

Atherosclerosis is a common feature of autogenous vein bypass grafts resulting in their long-term failure. Arterial pressure-induced distension is thought to play a major role in the wall thickening of vein grafts, which may in turn favor atherosclerotic complications. In this study, we evaluated the influence of vein distension on the development of atherosclerotic lesions in jugular vein grafts interposed into the common carotid arteries of rabbits. The proximal half of each vein graft was wrapped with a 4-mm-diameter polytetrafluoroethylene graft that reduced the vein graft diameter by 46 +/- 5%. Fourteen animals were fed a 1% cholesterol-rich diet for 8 weeks, and five animals were fed a normal diet. In normocholesterolemic and hypercholesterolemic animals, the wall thickness and the total cross-sectional area were significantly reduced in wrapped compared with unwrapped segments. Foam cells were never observed in normocholesterolemic animals. In hypercholesterolemic rabbits, the sudanophilic lesions covered 62 +/- 4% of the luminal surface in unwrapped segments and 31 +/- 7% in wrapped segments (p < 0.0001). In transverse sections, the surface areas of foam cells were also markedly reduced in wrapped compared with unwrapped segments. Reduction of the wall distension using a rigid external support protected the vein grafts from atherosclerosis, possibly as a result of the decrease in wall thickening that occurred in response to arterialization.

Analysis of Variance↗
PubMed1993

[Effects of de-endothelialization and angiotensin II on the vascular remodeling in a model of rabbit aorta organ culture].

The effects of de-endothelialization and angiotensin II (A II) on smooth muscle cell (SMC) growth are still controversial. Cell culture experiments suggest an hypertrophic effect of AII, whereas in vivo experiments in de-endothelialized arteries using angiotensin converting enzyme inhibitors suggest a possible role of AII on proliferation and/or migration of SMC. Phenotype of SMC in culture does not necessarily reflect that in the whole organ. Yet, in vivo models are too complex to permit conclusions as to the proper effect of AII or endothelium. Therefore, we examined the effect of de-endothelialization and AII on SMC growth in an organ culture of vessel wall. Rabbit thoracic descending aortas (n = 42) held at their in vivo length, perfused at 40 ml/min and pressurized to 70 mmHg (P70) were maintained in DME medium supplemented with 20% fetal calf serum for periods of time varying between 0 and 15 days. In another group (n = 26), aortas were relaxed and not pressurized (P0). In each group, some arteries were de-endothelialized; 21 arteries were exposed to AII (10(-6) M) and indomethacin (10(-5) M) during the incubation. SMC proliferation was evaluated by 3H-thymidine uptake by the vessel wall. Statistics were performed using covariance analysis. In P0 group, de-endothelialization or AII had no effect on the vessel wall. In P70 group, de-endothelialization or led to a significant increase in media area which was reported to extracellular matrix synthesis and in 3H-thymidine uptake (p < 0.005) which peaked at 3-5 days and returned to basis levels at 6-8 days. All had no effect on 3H-thymidine uptake (p = 0.516) in P70 group. Our results obtained in rabbit aortic organ culture suggest that de-endothelialization induces SMC growth depending on pressure and/or wall stretching. AII, per se, had no additional effect on SMC growth in this model.

Angiotensin II↗
PubMed1993

[Mechanisms of vascular hypertrophy in hypertension].

In hypertension, the thickening of the arterial wall by an increase in the cellular mass and collagen and elastin content may be considered to be an adaptive response to the high blood pressure. Positive and negative feedback systems play a role in the hypertension-vascular hypertrophy couple. Increased wall stress associated with stretching of the smooth muscle acts as a mechanical agonist of cellular growth in synergy with plasma or autocrine growth factors. In general, vascular hypertrophy ceases when the stress returns to normal. However, the increase in cell mass may result in an increase in systemic vascular resistance due to muscular hypertonicity and lead to an amplification of the hypertensive condition. The mechanisms of mechano-transduction are not fully understood. Moreover, genetic vascular changes affecting the structure of the vessels, the sensitivity to vasoactive substances or the geometry of the vascular system can also induce hypertension.

Angiotensin II↗
PubMed1992

Albumin transport characteristics of rat aorta in early phase of hypertension.

The effects of early-stage hypertension on the macromolecular transport characteristics of the aorta have been investigated in rats 1 week after the ligature of the abdominal aorta between the two renal arteries. The animals were left untreated or treated for 1 week with an angiotensin converting enzyme inhibitor (enalapril, 6 mg/kg per day). Blood pressure of a subgroup of hypertensive rats was acutely lowered to a normal level by injection of enalaprilat (1.5 mg/kg) at the time of the experiment. 131I-Albumin and 125I-albumin were injected 90 minutes and 5 minutes, respectively, before the rats were killed. The transmural distribution of the relative tissue concentrations across the wall was obtained using a serial frozen-section technique. Short-term albumin uptake permitted calculation of apparent endothelial permeability coefficients, and 90-minute uptake was used to estimate the steady-state albumin distribution within the media. The effect of early-stage hypertension on the characteristics of the arterial macromolecular transport depended on the aortic site; the ascending aortic arch appeared not to be affected. In the thoracic and abdominal aorta, the endothelial permeability coefficients increased significantly in hypertensive rats. This increase was not a direct effect of the arterial pressure, since the values were not significantly different when the pressure was acutely normalized. The 90-minute albumin concentration in the media was enhanced in hypertensive rats and returned to the normal value by acutely lowering the blood pressure, indicating that the increase observed in hypertensive rats resulted from a direct effect of pressure, possibly increased pressure-driven convection and/or pressure-induced stretching of the wall. Treatment by angiotensin converting enzyme inhibitor prevented hypertension and protected against its effects in hypertensive animals.

Albumins↗
PubMed1992

Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.

Inflammatory mediators released by macrophages (M phi) are believed to be involved in septic vasoplegia. To investigate the effect of M phi on vascular reactivity, excised rabbit carotids were exposed intraluminally either to peritoneal rabbit M phi, activated by 18 h of incubation with 1 microgram/ml lipopolysaccharide, or to the supernatants (SPN) derived from them. The contractile responses to phenylephrine (PE, 10(-6) M) were determined by measuring changes in diameter using an ultrasonic microdimensiometer 1, 2, and 3 h after the first control contraction. In control arteries (n = 12), PE-induced contractions were, respectively, 102.9 +/- 3.3%, 95.2 +/- 4.1%, and 89.7 +/- 3.8% of the first contraction, after 1, 2, and 3 h. Activated M phi significantly reduced PE-stimulated contractions after as little as 1 h of carotid exposure (percentage of controls at 1, 2, or 3 h: 74.1 +/- 5.6, 57.2 +/- 5.2, and 34.2 +/- 5.6, n = 10, P less than 0.001). The activated macrophage-derived SPN took longer to diminish carotid contractility than the M phi themselves, and became significant only after 2 h. The greater effect of M phi might be due to cooperation between M phi and vascular cells, as suggested by the amplified interleukin-1 release observed after M phi infusion. The presence of the endothelium partially protected carotid contractility from depression by activated M phi. Extraluminal addition of NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis prevented this depression in arteries with or without endothelium. No products of the oxidative pathway of L-arginine were detected in rabbit activated M phi. These results suggest that activation of this pathway in smooth muscle cells seems to be involved in vascular hypocontractility.

Animals↗
PubMed1992

[Reduction of atherogenesis in an arterialized venous graft by using an external sleeve].

The parietal thickening of a vein under hemodynamical conditions in the arterial system can be reduced when supporting the vein with a rigid external sleeve. To assess the role of thickness reduction in atherogenesis of an arterialized vein graft, a 4 mm thick external sleeve was implemented around the proximal half of a carotid-carotid vein graft in 16 New Zealand rabbits. Eleven rabbits were submitted to a hypercholesterolemic diet (HC group), while five others were submitted to a normal cholesterol diet (NC group). After eight weeks, a statistically significant difference in thickness was observed between free and sleeved segments, in the NC group with 105 +/- 9 microns versus 65 +/- 6 microns (p < 10.0001) respectively as well as in the HC group with 180 +/- 37 microns versus 99 +/- 35 microns (p < 10.0001) respectively. Studying the extent of soudanophilic lesions showed a statistically significant difference according to the use or not of an external sleeve where average extent is 68 +/- 17% in free segments versus 31 +/- 26% (p < 10.0001) is sleeved segments. The reduction in vein overfullness using an external constrictive sleeve prevents structural parietal changes in the vein and allows reducing atherogenesis of the arterialized vein graft.

Animals↗
PubMed1992

In vitro assessment of diameter-pressure relationship in carotid arteries from normotensive and spontaneously hypertensive rats.

OBJECTIVE: To compare the mechanical properties of carotid arteries from normotensive and spontaneously hypertensive rats. DESIGN: The pressure-diameter relationships of carotid arteries from nine normotensive adult Wistar-Kyoto (WKY) and nine spontaneously hypertensive rats (SHR) were measured in vitro under control conditions and after poisoning the smooth muscle cells with potassium cyanide. METHODS: Changes in diameter due to changes in transmural pressure were determined with an ultrasonic dimensiometer (12 MHz). The diameter values were determined from the transit times of the pair of echoes given by the proximal and distal walls. The carotid artery was submitted to stepwise increases in pressure of 25 mmHg, from 0 to 200 mmHg; each pressure level was maintained for 5 min before the arterial diameter was recorded. RESULTS: The carotid artery pressure-diameter relationship was a sigmoid curve in both strains. At the same level of pressure, the diameter of the carotid artery from SHR was significantly larger than that from normotensive rats (P < 0.05). Furthermore, the diameter values measured at the operating mean arterial pressure (roughly 100 mmHg for WKY rats and 150 mmHg for SHR) were markedly different (P < 0.001). In both strains, the diameter under passive conditions (with potassium cyanide) was significantly larger than that measured under control conditions (P < 0.01). CONCLUSIONS: Carotid arteries from SHR were significantly stiffer than those from WKY rats. Due to the pressure-dependency of the arterial wall stiffness, the increased arterial stiffness reported in hypertensive rats in vivo is related to an increase in distending arterial pressure and also to a significant reduction in the intrinsic compliance of the arterial wall.

Animals↗
PubMed1992

[Atherosclerosis of an arterialized venous graft. Reduction by rigid external support].

Vein grafts undergo early intimal thickening and accelerated atherosclerosis. To assess the role of increased wall stress and distension in the pathogenic responses, 11 New Zealand white rabbits underwent interposition of an autologous jugular vein graft in the left common carotid artery. To relieve wall stress and reduce distension, the half proximal part of the vein was wrapped with a polytetrafluoroethylene graft (i.d. 4 mm). Animals were fed 1% cholesterol for 8 weeks. Vein graft and carotid artery were perfusion fixed with Karnovsky solution at 100 mmHg. They were stained with Sudan IV, and 5-microns cross sections were stained with hematoxylin-eosin and orcein. The internal diameter was reduced by 46 +/- 10% in wrapped vein graft segments as compared with unwrapped ones. The percentage of luminal surface covered by sudanophilic lesions (%AS) was assessed by automatic planimetry. Results (mean +/- SD) were as follows. [table: see text]. Abundant foam cells were found in the intima of unwrapped veins, whereas they were absent or rare in wrapped segments. We concluded that atherosclerotic lesions could be prevented in vein grafts by reducing wall stress and distension.

Adaptation, Physiological↗
PubMed1991

Acute effects of tumor necrosis factor on the microcirculation in rat cremaster muscle.

The acute effects of TNF on the microcirculation were studied by in vivo microscopy in rat cremaster muscle. The changes in arteriolar diameter after topical administration of recombinant TNF (rTNF; 10(-4)-10(4) ng/ml) were studied in second-, third-, and fourth-order arterioles (A2-A4) whose mean diameters under control conditions were 64.3, 30.7, and 14.8 microns respectively. rTNF induced a concentration-dependent vasodilation whose amplitude was largest for the smallest arterioles. At the highest concentration tested, arteriolar diameter increased by 21, 29, and 41% of control diameter for the A2, A3, and A4 arterioles, respectively. Indomethacin or mefenamic acid, two structurally different prostaglandin synthesis inhibitors, markedly inhibited the degree of vasodilation induced by rTNF in the three arteriolar orders. As regards the effect of rTNF on vasoconstriction in response to norepinephrine, vasoconstriction was greatest for the smallest arterioles, and did not change 10 min after rTNF administration for any of the three arteriolar orders. We conclude that (a) rTNF has a direct vasodilatory effect which is greatest in the smallest arterioles, (b) this vasodilation is at least partly mediated by prostaglandins, and (c) administration of rTNF in itself does not acutely alter the response of the arterioles to vasopressive drugs.

Animals↗
PubMed1990

Phasic regional myocardial inflow and outflow: comparison of theory and experiments.

We developed a theory for regional blood flow in the beating heart and validated it with measurements of coronary arterial inflow and venous outflow in the open-chest anesthetized dog. The model used measured aortic, left ventricular, and coronary sinus pressures as input data under control conditions and during long diastoles induced by vagal stimulation. A nonlinear two-compartment lumped model for each transmural layer was obtained by spatial averaging a continuum description of the myocardial microcirculation based on morphometric measurements and appropriate fluid and vascular mechanics principles. The chief results and conclusions of the study are 1) an intramyocardial time constant on the order of 1 s is required to explain the phase opposition between inflow and outflow; 2) capillary and venous perfusion are in phase with arterial pressure, and arterial flow is out of phase with arterial pressure except in superficial intramural layers; 3) subendocardial retrograde systolic flow increases with increased contractility and time constants and decreased arterial pressure; and 4) endocardial capillary and venule volume change by 5.5 and 10%, respectively, during the control cardiac cycle.

Animals↗
PubMed1990

Effect of transmural pressure on low density lipoprotein and albumin transport and distribution across the intact arterial wall.

To investigate the effect of hyperpressure on the transport of low density lipoprotein (LDL) and albumin in the arterial wall, we measured in vitro the uptake of both iodine-131-labeled LDL and iodine-125-labeled albumin in intact rabbit thoracic aorta, held at in vivo length and pressurized to 70 or 160 mm Hg. Arteries were incubated for 2 hours (n = 8) at 70 mm Hg, and for 5 minutes (n = 4), 30 minutes (n = 4), 1 hour (n = 5), and 2 hours (n = 5) at 160 mm Hg. The transmural distribution of the relative concentrations of LDL (CLDL) and albumin (Calb) across the wall was determined by using a serial frozen sectioning technique. At 70 mm Hg, the mean medial CLDL and Calb values were 0.0018 +/- 0.0007 and 0.0039 +/- 0.0013, respectively. At 160 mm Hg, CLDL and Calb were markedly increased. The distribution of labeled albumin was almost uniform across the media and reached a steady state after 30 minutes, whereas labeled LDL accumulated in the first inner layers, a steady state being achieved after 1 hour. The 1-hour values of CLDL in the first and second luminal sections (0.24 +/- 0.03 and 0.13 +/- 0.05, respectively) were much higher than those of Calb, the CLDL/Calb ratios being 4.12 +/- 0.94 and 2.34 +/- 0.42 (p less than 0.01), respectively. In the subsequent sections, the CLDL decreased markedly and became much lower than the Calb, the CLDL/Calb ratio averaging 0.2 in the two-thirds outer media. To investigate whether LDL was trapped at high pressure in the inner layers, vessels were exposed to a tracer-free intraluminal solution for 30 minutes, after a 30-minute incubation with tracers. After washout, albumin was almost totally removed from the wall, while the CLDL were practically unchanged. Compaction of the media induced by high distending stresses applied to the vessel might have hindered the efflux of LDL, whereas albumin moved freely through the wall. Synergy between increased endothelial permeability and compaction of the media together with enhanced pressure-driven convection might account for the marked increase in LDL concentration observed in the inner wall at high pressure.

Animals↗
PubMed1990

[Measurement of water, DNA and collagen in different parts of the aorta in rats. Effect of hypertension].

Renovascular hypertension was induced in two-week rats (group HR, n = 6) and their aortas were studied 8 weeks later and compared with those from normotensive rats (group NR, n = 6). Total water content, DNA (fluorometric method) and collagen (calculated from hydroxyproline concentrations) concentrations were measured in the media of the arch, the descending thoracic aorta and the abdominal aorta. Water content and DNA content did not significantly change in the different parts of the aorta. The collagen content significantly decreased from the arch to the abdominal aorta, in NR as well as in HR group (p less than 0.01). Hypertension did not affect water content, DNA neither collagen content in the abdominal aorta. In the arch and in the descending thoracic aorta, hypertension was associated with an increase in collagen content (p less than 0.001), whereas the water and DNA contents did not significantly change. These results suggest that hypertension induced an increased collagen synthesis only in the thoracic aorta, this being more important in the arch than in the descending thoracic aorta. Responses to hypertension are different in thoracic and in abdominal part of rat aorta.

Animals↗
PubMed1990

[Effects of arterial hyperpression on the transport and distribution of LDL and albumin in the arterial wall].

To investigate the effect of hyperpressure on the transport of LDL and albumin in the arterial wall, we measured in vitro the uptake of both 131I-LDL and 125I-albumin in intact rabbit thoracic aorta, held at in vivo length and pressurized to 70 or 160 mmHg. Arteries were incubated for 2 h at 70 mmHg, and for 5 min, 30 min, 1 h and 2 h at 160 mmHg. The transmural distribution of the relative concentrations of LDL (CLDL) and albumin (CAlb) across the wall was determined using a serial frozen sectioning technique. At 70 mmHg, the mean medial CLDL and CAlb values were 0.0018 +/- 0.0007 and 0.0039 +/- 0.0013, respectively. At 160 mmHg, CLDL and CAlb were markedly increased. The distribution of labeled albumin was almost uniform across the media and reached a steady state after 30 min, whereas labeled LDL accumulated in the first inner layers, a steady state being achieved after 1 h. The 1-hour values of CLDL in the first and second luminal sections (0.24 +/- 0.03 and 0.13 +/- 0.05, respectively) were much higher than those of CAlb, the CLDL/CAlb ratios being 4.12 +/- 0.94 and 2.34 +/- 0.42 (p less than 0.01), respectively. In the subsequent sections, the CLDL markedly decreased and became much lower than the CAlb, the CLDL/CAlb ratio averaging 0.2 in the two thirds outer media. To investigate whether LDL was trapped at high pressure in the inner layers, vessels were exposed to a tracer-free intraluminal solution for 30 min, following a 30-minute incubation with tracers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Vascular smooth muscle fibers and the autonomic nervous system].

Vascular Smooth Muscle cell (V.S.M.C) plays a major role in the regulation of vasomotion. Sympathetic system play a key role in vascular smooth muscle function. Epinephrine (humoral pathway) and norepinephrine (nervous pathway) can both stimulate V.S.C.M. via delta and beta adrenergic receptors. The function of parasympathetic system is more controversial. Acetylcholine induces the release of a relaxing factor by the endothelial cell (E.D.R.F.) but it has a direct contracting effect on V.S.C.M. Neural vasodilation is also concerned by noradrenergic mechanisms.

Autonomic Nervous System↗
PubMed1989

Asymmetry of Doppler spectrum in stenosis differentiation.

The asymmetry of the spectral distribution of ultrasonic Doppler flow velocity signals, assessed using the coefficient of skewness, is discussed as a criterion of stenosis differentiation. Its performance is compared with that of the index of turbulence intensity for both in vitro and in vivo flow Doppler signals, recorded distal to a stenosis. The power spectral distributions are computed using the direct Fourier transform and maximum likelihood method. The asymmetry of spectral distribution has proved to be a more efficient criterion than the turbulence intensity. The maximum likelihood method ensures better stenosis differentiation than the direct FFT method.

Animals↗
PubMed1989

Role of LDL receptors in the in vitro uptake and degradation of LDL in the media of rabbit thoracic aorta.

The possible role of plasma low-density protein (LDL) receptors in the uptake and degradation of LDL in the whole arterial wall was investigated by comparison of the in vitro uptake of 125I-native LDL (nLDL) and 131I-methylated LDL (mLDL) by the media of deendothelialized rabbit thoracic aorta excised at in vivo length and pressurized to 70 mm Hg, taking the advantage that mLDL is not recognized by the LDL receptor. The distribution of the relative concentrations of nLDL (Cn) and mLDL (Cm) across the wall was obtained using a serial frozen sectioning technique. The aorta was incubated under three different conditions for varying periods of incubation in order to analyze separately the processes of binding, binding-internalization, and degradation. At 39 degrees C, in which binding-internalization and degradation occurred, Cn was significantly higher than Cm at each position across the media. The mean medial Cn/Cm ratio was 1.36 +/- 0.15 (n = 5) after 1 hour of incubation, and decreased to 1.23 +/- 0.22 (n = 7) after 2 hours of incubation and to 1.13 +/- 0.11 (n = 5) after 4 hours of incubation. At 4 degrees C, in which internalization and degradation were blocked, the Cn/Cm ratio reflected the surface nLDL binding alone; the Cn/Cm ratio was 1.47 +/- 0.20 (n = 5) after 4 hours of incubation, higher than the value obtained at 39 degrees C. To investigate whether degradation of nLDL occurred after receptor binding, the interstitial LDL was washed out by an LDL-free solution after 2-hour incubation at 39 degrees C. After 30 minutes of washout, the Cn/Cm ratio decreased to 1.06 +/- 0.20 (n = 5) in the inner media and was unchanged in the outer media. After 1 hour of washout, the ratio declined to 0.57 +/- 0.18 (n = 7) in the inner part of the media and increased progressively to 1 at the media-adventitia boundary. The Cn/Cm ratio, at 0.67 +/- 0.12 (n = 5), was practically constant throughout the media after 2 hours of washout. The nLDL degradation rate across the media was obtained from the comparison of nLDL and mLDL before and after the washout. A steep decreasing gradient in nLDL degradation rate was observed from the luminal to the external surface. The mean medial nLDL degradation rate value was 9.6 +/- 4.5 microliters/cm3 wet tissue/hr. We concluded that functional LDL receptors participate in the uptake and degradation of LDL in the whole aorta.

Analysis of Variance↗
PubMed1989

[Effects of transmural pressure on the transport and distribution of low density lipoproteins in the arterial wall].

In an attempt to investigate the effects of transmural pressure on LDL transport and distribution across the arterial wall, uptake of labeled LDL has been measured in excised rabbit thoracic aorta, held at in vivo length and pressurized to 70 or 160 mmHg. The transmural distribution of LDL concentration across the wall was determined by examining serial frozen sections cut parallel to the luminal surface at 20 microns intervals from the intima to adventitia. The LDL concentration observed in the first luminal section at 160 mmHg was 20-fold higher than that obtained at 70 mmHg. The LDL concentrations decreased in the subsequent sections of the first half of the media and became similar, in the outer half of the media, to the values observed under normal pressure. These results might provide an account of one of the mechanisms involved in the deleterious effects of hypertension in atherogenesis.

Animals↗