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M Duriez

Publications and source records attributed to M Duriez.

35 records · Page 2Linked to original sources
PubMed1995

Structural changes and in situ aortic pressure-diameter relationship in long-term chemical-sympathectomized rats.

This study determined the effects of long-term chemical sympathectomy with guanethidine (GN) on the mechanical properties and composition of the distal abdominal aorta in Wistar rats. GN was daily administered for 3 mo (3M-GN, from 1 to 12 wk), 5 wk (5W-GN, from 7 to 12 wk), and 8 days (8D-GN, from 11 to 12 wk). All experiments were performed at 12 wk of age to avoid age differences at examination. We used a high-resolution echo-tracking system to determine in situ, in the systolic-diastolic range, the aortic diameter-, compliance-, and distensibility-pressure curves in anesthetized rats. We observed an equivalent significant fall in the tyramine pressor response in all conscious GN-treated rats. Blood pressure was not affected by sympathectomy after 8 days and 5 wk of treatment but was significantly reduced in 3M-GN rats. Chronic sympathetic denervation increased aortic diameter and compliance in 8D-GN rats, compared with those obtained at the same distending pressure in control rats, suggesting vascular smooth muscle relaxation. In contrast, in 5W-GN and 3M-GN rats, the distensibility pressure-curves were significantly shifted toward lower levels of distensibility and pressure, indicating a decreased aortic distensibility at the same level of arterial pressure. Sympathectomy produced a significant reduction in the content of elastin, one of the most distensible components of the arterial wall in 5W-GN and 3M-GN rats. These results suggest that intact sympathetic nerves are necessary to maintain normal functional and structural properties of large arteries in rat. The reduction in aortic distensibility, in long-term sympathectomized rats, could have resulted from complex interactions between local aortic denervation, change in the set point of distending pressure, and changes in aortic smooth muscle tone and/or wall composition.

Animals↗
PubMed1994

Effect of chronic dihydropyridine (isradipine) on the large arterial walls of spontaneously hypertensive rats.

BACKGROUND: The effect of genetic hypertension and of chronic therapy by calcium entry blocker (CEB, isradipine) on the function and structure of large arteries has been studied in adult spontaneously hypertensive rats (SHR, n = 30) and in their normotensive control Wistar-Kyoto (WKY) rats (n = 30). METHODS AND RESULTS: Fifteen-week-old rats were randomly allocated to treatment with isradipine (3 mg/kg subcutaneously once a day) or to placebo and followed for 12 weeks. Hemodynamic parameters, including instantaneous pressure and aortic velocity, were recorded under anesthesia at the end of the treatment period. Passive mechanical properties of carotid arteries were measured in situ in the presence or the absence of smooth muscle cell activity (potassium cyanide poisoning). Histomorphometric parameters of the carotid and aortic media, including cross-sectional area, medial thickness, nucleus density and size, and medial contents of proteins of interstitial matrix, were measured by an automated morphometric system. Untreated SHRs had greater peripheral resistance, stiffer and thicker arterial walls because of smooth muscle cell hyperplasia (thoracic aorta and carotid artery) and/or hypertrophy (thoracic aorta), and increased collagen content than did normotensive control rats. SHRs showed a significant left ventricular hypertrophy. For the whole duration of treatment, treatment with CEB normalized the arterial pressure in SHRs. We observed a significant decrease in peripheral resistance, increased cardiac output, and left ventricular contractility without significant reduction in left ventricular hypertrophy. Increases in diuresis and natriuresis were associated during the last week of treatment in both treated strains with marked increase in plasma renin activity; in contrast, urinary aldosterone was increased by treatment in WKY rats but not in SHRs. Arterial compliance was significantly increased by CEB under control and passive conditions. CEB induced a significant reduction in the medial hypertrophy of the aortic walls of SHRs and WKY rats associated with a reduction in medial hyperplasia. In the carotid artery, CEB reduced smooth muscle cell hypertrophy but did not affect the smooth muscle cell hyperplasia. Isradipine significantly reduced the arterial wall collagen contents in both strains, with marked increases in the elastin content in the carotid but not in the aortic wall. CONCLUSIONS: These results suggest that (1) despite normalization of arterial pressure, chronic treatment with CEB in SHRs does not significantly reduce left ventricular hypertrophy, probably because of increase in myocardial contractility and/or increase in plasma renin activity; (2) mechanical properties of the arterial wall are normalized by treatment; and (3) remodeling of the arterial wall by CEB is not uniform according to the studied vessel.

Animals↗
PubMed1994

Angiotensin converting enzyme inhibition prevents the increase in aortic collagen in rats.

Four groups of 4-week-old spontaneously hypertensive rats were treated during 4 months with the angiotensin converting enzyme inhibitor quinapril at 1 mg/kg per day (Q1) or 10 mg/kg per day (Q10), hydralazine at 15 mg/kg per day (H), or placebo (P). In the first set of experiments, blood pressure was measured in conscious rats, and plasma and aortic angiotensin converting enzyme activities were evaluated. In the second set of experiments, histomorphometric parameters of the thoracic aorta were evaluated. Mean blood pressure was lower in the Q10 and H groups (136 +/- 16 and 149 +/- 11 mm Hg) compared with the P group (190 +/- 23 mm Hg) (P < .01). The Q1 group showed mean blood pressure values (171 +/- 15 mm Hg) lower than the P group (P < .05) but significantly higher than the Q10 and H groups (P < .01 and P < .05, respectively). Aortic medial cross-sectional area was significantly lower in the H and Q10 groups (455 +/- 61 and 487 +/- 57 x 10(3) microns 2) than in the P group (636 +/- 72 x 10(3) microns 2) (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Additive and synergistic effects of a low-molecular-weight, heparin-like molecule and low doses of cyclosporin in preventing arterial graft rejection in rats.

Arteriosclerotic intimal proliferation is one of the main long-term complications of organ transplantation. Low-molecular-weight, heparin-like molecules prevent myointimal proliferation in arterial wall injury and limit rejection in skin allografts. Cyclosporin limits rejection but has no major effect on intimal proliferation. Therefore, an experimental protocol was designed to test whether heparin-like molecules interacted with low doses of cyclosporin to prevent arterial wall immune system injury and response in a model of arterial graft rejection in normotensive and hypertensive rats. Aortic allografts were performed in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) normotensive control rats. Four groups of 10 allografted (SHR and WKY) rats were used: one group was treated with placebo, one with low doses of cyclosporin (2 mg/kg body wt per day), one with low-molecular-weight, heparin-like molecule (1 mg/kg body wt per hour), and one with low doses of cyclosporin plus low-molecular-weight, heparin-like molecule. Ten SHRs and 10 WKYs were isografted and served as the control groups. All rats were killed 8 weeks after aortic grafting. Structural parameters of the grafted segment were measured by morphometric analysis on formalin-fixed sections with specific stains. The classical signs of immune system injury and response were present in the untreated allografts in SHRs and WKYs: inflammatory infiltration of the adventitia, medial injury, and intimal proliferative response. Low doses of cyclosporin had a significant beneficial effect on immune medial injury by increasing medial thickness and the number of remaining smooth muscle cells and decreasing the extracellular matrix injury. Cyclosporin had no protective effect on intimal proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

Effect of a nonhypotensive long-term infusion of ANP on the mechanical and structural properties of the arterial wall in Wistar-Kyoto and spontaneously hypertensive rats.

A nonhypotensive dose of atrial natriuretic peptide (ANP) was infused (60 pg/kg body wt per day s.c. by osmotic pump) for 25 days in 16-week-old normotensive Wistar-Kyoto rats (WKYs, n = 12) and age-matched spontaneously hypertensive rats (SHRs, n = 12). During the infusion period, systolic blood pressure, urinary volume, and cyclic guanosine monophosphate (cGMP) excretion/12 hr were measured once a week in both groups. Then mechanical and morphological properties of the arterial wall and plasma ANP levels were assessed and compared with those from control groups of SHRs (n = 8) and WKYs (n = 8) receiving a saline vehicle. The compliance (CC) of the in situ localized carotid artery was measured for pressures ranging from 25 to 175 mm Hg under control conditions and after "poisoning" of smooth muscle tone by potassium cyanide. After pressure fixation, the medial thickness, elastin and collagen contents, and the size and number of nuclei were measured in the thoracic descending aorta. In WKYs, ANP did not modify either mechanical or structural properties of the arterial wall or biochemical parameters. Conversely, in ANP-treated SHRs, CC was significantly increased compared with untreated SHRs under basal conditions (p < 0.03) and after potassium cyanide poisoning (p < 0.02). Structural properties were also modified by ANP in SHRs, i.e., medial thickness (129.3 +/- 4.1 versus 113.1 +/- 3.3 microns, p < 0.01) and nuclear size (8.81 +/- 0.28 versus 5.52 +/- 0.20 microns 2, p < 0.0001) in untreated and treated SHRs, respectively. Furthermore, urinary volume and cGMP content were significantly increased during ANP infusion in treated SHRs (p < 0.05). The present results indicate concomitant modifications of mechanical and structural properties of the arterial wall in SHRs chronically treated with low doses of ANP. These long-term effects of ANP could be involved in the remodeling of the arterial wall observed during hypertension and could have beneficial effects on cardiovascular diseases in chronic sustained hypertension.

Animals↗
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↗
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

Effect of converting enzyme inhibition on allograft-induced arterial wall injury and response.

Converting enzyme inhibition (CEI) can prevent myointimal proliferation after arterial wall balloon injury. Because intimal proliferation is the main long-term complication of chronic vascular rejection, we tested the effect of CEI (perindopril, 1 mg/kg twice a day) on arterial rejection-induced intimal proliferation, using a model of aortic allograft in normotensive Wistar-Kyoto and spontaneously hypertensive rats. Eight-week-old rats were grafted and studied 2 months later. The structural parameters of the transplanted aortic wall were measured by morphometric analysis of specifically stained, formol-fixed sections. CEI did not prevent adventitial inflammatory infiltration but significantly increased the number of living cells and prevented the partial destruction of elastic laminae in the media, thereby increasing medial thickness to close to that of sham-operated controls. CEI significantly decreased intimal thickness and intimal collagen density, without changing the absolute number of intimal smooth muscle cells. The intimal thickness and the intimal collagen density were significantly correlated with the effect of CEI on blood pressure. CEI partially prevented the consequences of immune injury to the media within the arterial wall, probably by suppressing the proinflammatory activity of angiotensin II. It also decreased the recipient arterial wall response by acting more on the trophicity of intimal cells and on their ability to produce collagen rather than by directly inhibiting smooth muscle cell proliferation in our model of arterial allograft.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Reduction of energy required for defibrillation by delivering shocks in orthogonal directions in the dog.

Reduction of energy required to defibrillate (ERD) seems to represent a necessary condition for intensive development of implantable defibrillator, so as for minimization of cardiac and pulmonary damages provoked by high energy transthoracic defibrillation electric shocks. The present work describes a defibrillation method using shocks delivered in orthogonal directions and separated by a 100 ms delay. Defibrillation threshold measured with classical unidirectional shocks on 30 dogs has been found to be 286.8 +/- 22.2 joules. In the same animals, defibrillation threshold measured by use of orthogonal shocks has been found to be 101.4 +/- 14.9 joules. We conclude that this crossed shocks method leads to a substantial reduction of ERD (64%).

Animals↗
PubMed1985

Relationships between single-vessel coronary artery obstructions and wall motion dysfunction analyzed by four computer-based methods.

We analyzed regional wall motion in 238 patients by using cineangiograms recorded in the 30 degrees right anterior oblique projection. The sample was divided into three groups: a normal group (n = 71), a group with isolated obstruction of the left anterior descending coronary artery and previous anterior myocardial infarction (n = 85), and a group with isolated obstruction of the right coronary artery and previous inferior myocardial infarction (n = 82). Both anterior and inferior groups also had motion abnormality within the corresponding anterior or inferior wall as judged by the qualitative analysis of cineangiograms. Four quantitative methods were compared: a long axis method and a center of mass method using internal reference systems, a method derived from the Stanford model and an area-based method using external reference systems. Normal regional values were determined from the normal group to evaluate the specificity and sensitivity of the methods. The area-based method was the most sensitive in the anterior infarction group, whereas the center of mass method was the most sensitive in the inferior infarction group. We conclude that there is no evidence that any method, among those tested, is superior to others for every expected location of wall motion abnormality.

Adult↗
PubMed1977

[Sexual cycle period and resistance of mice to acute experimental hypoxia].

Variations of survival to an acute hypoxia (nitrogen) were studied, in 200 females, OF1, SPF mice, 72 days old, in groups of 10, at different periods of their estrus cycle, which were evidenced by vaginal smears. In mice which were in diestrus since 3-4 following days, the hypoxic survival (27.27%) was statistically less than in mice which were in estrus (58.00 %) or at the beginning of the diestrus (53.85 %).

Animals↗
PubMed1975

[Influence of recent modification of behavioral relationships of male and female OF1 mice on resistance to nitrogen or carbon monoxide hypoxia].

A decrease of resistance to hypoxia is obtained in OF1 mice, 24 hours after an hyperactivity resulting from a grouping by 13 of male or female mice previously isolated. Besides, this decrease is statistically significant in an acute nitrogen hypoxia but not in an acute carbon monoxide poisoning. In both hypoxias, in mice of same age the males are less resistant than females.

Age Factors↗
PubMedDate not supplied

Cardiac functional improvement by a human Bcl-2 transgene in a mouse model of ischemia/reperfusion injury.

BACKGROUND: Apoptosis has been shown to contribute to myocardial reperfusion injury. It has been suggested that, in reducing the apoptotic component within the ischemic area at risk, Bcl-2 overexpression could lead to a ventricular function improvement. METHODS: Transgenic mice overexpressing the anti-apoptotic human Bcl-2 cDNA in heart were subjected to a 1-h left coronary artery occlusion followed by a 24-h reperfusion. At the end of the experiment, left ventricular function was assessed by two-dimensional echocardiography. After sacrifice, the area at risk (AR) and the infarct area (IA) were determined by Evans blue and triphenyltetrazolium chloride staining, respectively. The extent of apoptosis was assessed by the TUNEL method. Non-transgenic littermates served as controls. RESULTS: Baseline AR was not different between Bcl-2 transgenic mice and their wild-type littermates. In contrast, left ventricular ejection fraction was significantly improved in the transgenic mice line (61.25 +/- 4.0%) compared to non-transgenic littermates (43.2 +/- 5.0%, p < 0.01). This functional amelioration was correlated with a significant reduction of infarct size in transgenic animals (IA/AR 18.51 +/- 3.4% vs 50.83 +/- 8.4% in non-transgenic littermates). Finally, apoptotic nuclei were less numerous in transgenic mice than in controls as quantified by TUNEL analysis (8.1 +/- 2.2% vs 20.6 +/- 4.4%). CONCLUSIONS: Bcl-2 overexpression is effective in reducing myocardial reperfusion injury and improving heart function. This benefit correlates with a reduction of cardiomyocyte apoptosis. The apoptotic component of ischemia/reperfusion injury could therefore constitute a new therapeutic target in the acute phase of myocardial infarction.

Animals↗
PubMedDate not supplied

Endothelium-dependent changes in arterial diameter in old normotensive rats.

1. In normotensive rats, removal of carotid artery endothelium results in an acute increase in diameter. This finding, observed in young animals, has not been investigated in old animals. The present study was undertaken to assess the contribution of endothelial function in the regulation of arterial stiffness in aged rats. 2. In normotensive female WAG/Rij rats, isobaric (100 mmHg transmural pressure) carotid diameter was measured in vitro in situ, using a previously described arterial preparation associated with a high-resolution echotracking technique allowing non-invasive diameter measurements under baseline conditions, after removal of the endothelium and after total relaxation of vascular smooth muscle by potassium cyanide. Histomorphometry of the carotid wall was studied after pressure fixation (100 mmHg) of the arteries. 3. Compared with younger animals (10 months), older animals (30 months) had the same baseline carotid isobaric diameter but significantly higher values of wall thickness and collagen content. In older animals, whereas total relaxation by potassium cyanide was associated with a slight but significant increase of isobaric diameter, no increase was observed after endothelium removal. 4. The results of the presnt study provide evidence that, in old normotensive rats, endothelium-dependent increases in isobaric carotid diameter are blunted. This endothelium alteration may contribute to the age-dependent increase in isobaric carotid stiffness observed in old rats.

Aging↗