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Biomedical subjects

L Capron

Publications and source records attributed to L Capron.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Description and mechanisms of sclerotic arterial diseases of the lower limbs].

Sclerotic involvement of abdominal aorta and lower limb arteries is related to 2 types of fundamental lesions: atherosclerosis and arteriosclerosis. Atherosclerosis is a focal intimal thickening (plaque) of large- and medium-sized arteries, which combines atheroma (lipid deposition) and fibrosis. Plaque rupture is the crucial event in the progression of atherosclerosis, directly causing most acute thrombotic events, and contributing in great part to plaque expansion. Arteriosclerosis is a diffuse fibrosis of the arterial wall with thickening of the intima, and thinning of the media. Two forms of arteriosclerosis probably exist with distinct mechanisms and consequences. Obliterating arteriosclerosis mainly involves leg arteries (causing poor distal run-off) and appears to be essentially enhanced by ageing, diabetes and chronic renal insufficiency. Dilating arteriosclerosis involves large arteries where it provokes aneurysm formation; it is related to ageing, but seems also to be dependent upon an inborn dystrophy of arterial connective tissue. These 3 components of sclerotic arterial diseases of the lower limbs are often combined in the same individual.

Arteries↗
PubMed1995

[Diagnosis of sclerotic arterial diseases of the lower limbs].

Diagnosis and treatment of lower limbs arterial disease do not depend exclusively on functional staging. Fontaine's classification has to be replaced by a classification based on clinical and complementary investigations to understand better the evolutive risks, and guide management. Distal systolic pressures along with symptom analysis and clinical examination allow a more precise diagnosis. Complementary investigations aim at assessing, the localization and extension of atherosclerotic lesions; the severity of tissue ischaemia. The concept of critical ischaemia has tried to insure greater diagnostic homogeneity for patients with rest ischaemia. The role of complementary investigation can only increase for the diagnosis and management sclerotic arterial disease. The detection of the other localizations of atherosclerosis and arteriosclerosis are essential to prevent complications which are responsible for the prognosis of the disease. Sclerotic arterial diseases represent approximately 90 to 95% of the causes of arterial diseases. Identification of these other causes remains, however, essential as it can greatly influence prognosis.

Arteries↗
PubMed1995

Heterogeneity in migration of smooth muscle cells from normal and injured rat thoracic aorta in primary culture.

OBJECTIVE: Aside from proliferation, migration of smooth muscle cells is an essential component of the arterial sclerotic reaction. The aim of this study was to define a model to study migration. METHODS: Primary cultures of smooth muscle cells were derived from normal or injured rat thoracic aorta. An image analysis system was used to track cells migrating out of the explants and measure the displacement of their centre of gravity. RESULTS: Migration speeds for smooth muscle cells randomly sampled from the normal whole media were very heterogeneous. The media were therefore separated into three vertical segments. Cells from the middle third migrated faster than those from the upper and lower thirds, regardless of whether they originated from the anterior and posterior parts of the segment (P = 0.001). Heparin (10 micrograms.ml-1) only inhibited smooth muscle cell migration from the middle segment (P < 0.001). Migration of smooth muscle cells from explants of aorta 3 and 14 d after injury was also studied using a balloon catheter. Three days after injury, cell velocity varied widely among the segments of the same media. In contrast, 14 d after injury cells from neointimal explants migrated homogeneously and at a slower rate than those obtained from normal media. CONCLUSIONS: These experiments show migratory variations among smooth muscle cells depending upon their position in the normal aorta and their state of activation after arterial injury. This variability must be taken into account when planning experiments to study smooth muscle cell migration.

Animals↗
PubMed1995

Pharmacologic approaches to the treatment of atherosclerotic arterial obstruction.

Three consecutive periods in the natural history of atherosclerosis are amenable to medical treatment. Plaque development is the main target of prevention, which also aims at slowing the progression of already existing plaques. The control of several established risk factors (high blood cholesterol, high blood pressure, diabetes mellitus, tobacco smoking) has already yielded encouraging benefits, especially in the field of secondary prevention. More efficient prophylaxis is to be expected, either from the further improved control of these classic risk factors with earlier, stronger, and longer interventions or from the correction of newly established causal determinants of atherosclerosis. A plaque manifests itself clinically through progressive or abrupt obstruction of the arterial lumen, which can be avoided or retarded by interventions aimed at reducing thrombosis, at controlling plaque instability (the major cause of thrombosis), and at enhancing arterial remodeling (which allows compensatory enlargement of the arterial lumen). When ischemia has occurred, a third wave of palliative treatments aims at improving energy supply to the organ with compromised vascularization. Classic treatments reduce oxygen consumption or improve oxygen extraction by ischemic tissues. In addition, the design of drugs to enhance the development of collateral channels appears to be promising therapeutic approach.

Animals↗
PubMed1995

National study of obliterative arterial disease of the lower limbs involving general practitioners in France: Artemio study.

A national survey was performed in France from May to June, 1993. The aim of this study was to evaluate general practitioners' attitudes and behaviors when diagnosing and managing patients with lower extremity arterial disease (LEAD). One thousand general practitioners, randomly drawn from an exhaustive list, were contacted to participate in a telephone interview concerning the last patient with intermittent claudication seen in their practice. Four hundred seventy-six general practitioners participated. Risk factors noted for these 476 patients with intermittent claudication were in agreement with the literature: 86% were men aged 64 +/- 10 years (mean +/- SD) and 14% were women aged 73 +/- 8 years. Sixty-two percent had a pain-free walking distance of between 100 and 500 meters at diagnosis. Forty-five percent were former smokers and 37% currently smoked; 55% had hypertension, 14% diabetes, and 56% disturbances of lipid metabolism. A majority of them were hypercholesterolemic. The diagnosis of the disease was based primarily on a clinical assessment, confirmed for 33% by Doppler or echo Doppler. The mean duration of diagnosis was 4.4 +/- 4.1 years. Management of the disease was mainly by prescription of vasodilators (91%), antiplatelet agents (59%), and anticoagulants (8%). Use of Doppler or echo Doppler was recommended once a year. Infection was observed in 27% of patients. Thirty-eight percent had had a cardiac incident (angina pectoris or myocardial infarction) and 10% a cerebrovascular accident. They differed significantly from those with LEAD alone for the following parameters: age (68.5 +/- 9.2 vs. 63.2 +/- 10.3 years; p < 0.001); duration of LEAD (5.6 +/- 4.6 vs. 3.6 +/- 3.5 years; p < 0.001); hypertension (65% vs. 50%; p < 0.01); and current smoking (29% vs. 43%; p < 0.01). This survey confirmed the feasibility of telephone interviewing, on a large sample of general practitioners in France. The high level of association with other cardiac incidents was, for these patients, a much higher risk of mortality and morbidity than LEAD alone. It would be interesting to validate the associations observed with a prospective study of comorbidity.

Adult↗
PubMed1995

Targeting platelets containing electro-encapsulated iloprost to balloon injured aorta in rats.

Drugs can be electro-encapsulated within platelets and targeted to damaged blood vessels by exploiting the platelet's natural haemostatic properties to adhere to collagen and other vessel wall constituents revealed by injury. A rat aorta balloon angioplasty model has been used to study the effect on platelet deposition of giving iloprost loaded platelets i.v. during the balloon injury. After labelling the circulating platelets with 111-Indium before balloon injury, time course studies showed maximum platelet deposition on the injured aorta occurred at about 1 h post-injury and the deposition remained stable over the next 2-3 h. When iloprost-loaded platelets were given i.v. during injury and the circulating platelet pool labelled with 111-Indium 30 min later, platelet deposition, measured at 2 h postinjury, was substantially and significantly reduced compared with control platelet treatment. Some anti-proliferative effects of iloprost-loaded platelets given i.v. during injury have also been observed. Whereas the incorporation of [3H]-thymidine into aorta intima-media DNA at 3 days post injury was 62-fold higher in balloon injured rats than in control sham operated rats, thymidine incorporation into intima/media of rats which had received iloprost loaded platelets during injury was reduced as compared with rats subjected only to the injury procedure. The reduction was only of near significance, however, but at 14 days after injury the total DNA content of the aorta intima/media of rats given iloprost loaded platelets during injury was significantly reduced. Although iloprost loaded platelets can clearly inhibit excessive platelet deposition, other encapsulated agents may have greater anti-proliferative effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗
PubMed1994

Advanced glycation end products (AGEs) on the surface of diabetic erythrocytes bind to the vessel wall via a specific receptor inducing oxidant stress in the vasculature: a link between surface-associated AGEs and diabetic complications.

Vascular complications are an important cause of morbidity and mortality in patients with diabetes. The extent of vascular complications has been linked statistically to enhanced adherence of diabetic erythrocytes to endothelial cells (ECs) and to the accumulation of a class of glycated proteins termed advanced glycation end products (AGEs). We hypothesized that formation of AGEs on the surface of diabetic erythrocytes could mediate their interaction with ECs leading to binding and induction of vascular dysfunction. Enhanced binding of diabetic erythrocytes to ECs was blocked by preincubation of erythrocytes with anti-AGE IgG or preincubation of ECs with antibodies to the receptor for AGE (RAGE). Immunoblotting of cultured human ECs and immunostaining of normal/diabetic human tissue confirmed the presence of RAGE in the vessel wall. Binding of diabetic erythrocytes to endothelium generated an oxidant stress, as measured by production of thiobarbituric acid-reactive substances (TBARS) and activation of the transcription factor NF-kappa B, both of which were blocked by probucol or anti-RAGE IgG. Erythrocytes from diabetic rats infused into normal rats had an accelerated, early phase of clearance that was prevented, in part, by antibody to RAGE. Liver tissue from rats infused with diabetic erythrocytes showed elevated levels of TBARS, which was prevented by pretreatment with anti-RAGE IgG or probucol. Thus, erythrocyte surface AGEs can function as ligands that interact with RAGE on endothelium. The extensive contact of diabetic erythrocytes bearing surface-associated AGEs with vessel wall RAGE could be important in the development of vascular complications.

Animals↗
PubMed1994

[The past, present and future of arterial infection].

Today, the pathology of large and medium-sized arteries is in most part considered as degenerative or inflammatory. The role of infection has been preponderant (syphilis) but has become quite modest now, restricted to infectious aneurysms. According to certain observations, infections may participate in initiating arterial inflammation, whether it be specific (Kawasaki's disease, Takayasu's arteritis, coronary artery disease of cardiac grafts) or less so ("plain" atherosclerosis). Suspected microbes (herpes viruses, Chlamydia pneumoniae, etc.) would damage the arterial wall either directly by infecting it, or indirectly by provoking an autoimmune reaction against some of its components (e.g. heat shock proteins). These hypotheses are worth serious consideration because, if established as correct, they would modify radically our etiologic, therapeutic and prophylactic conceptions of arterial diseases, including of course the main one, atherosclerosis.

Acquired Immunodeficiency Syndrome↗
PubMed1994

[Treatment of skin ulcers of venous origin].

Ulceration of the skin is the most severe complication of chronic venous insufficiency of the lower limbs. The ulcer reflects a profound impairment of the venous anatomy and function, often the late sequel to a deep venous thrombosis. The available surgical techniques are rarely apt to repair these lesions completely. Medical treatment is palliative, based upon the strict control of superficial venous hypertension (leg drainage and compression) and the rational use of local therapies (ulcer cleanliness, debridement and dressing). The physician must obtain the co-operation of the patient and the help of a competent nurse. Failures and recurrences are frequent. Rather than to hopeless resignation or even to abandon, such drawbacks should lead to a critical reassessment of each step in the treatment to identify imperfections, and to correct them.

Chronic Disease↗
PubMed1994

Effects of heparinoids on the sclerotic reaction of rat thoracic aorta to injury: comparison between standard and low-molecular-weight heparins in vitro and in vivo.

To assess further the influence of heparinoids on arterial sclerosis, we compared the effects of standard heparin and of a low-molecular-weight (low-mol-wt) heparin (CY 216) in vitro on proliferation of cultured arterial smooth muscle cells (SMC) from rat aorta and in vivo on the sclerotic response of rat thoracic aorta to injury with a balloon catheter (SMC proliferation and deposition of elastin and collagen in the intima-media, using biochemical and histomorphologic techniques). Both heparinoids decreased replication of SMC in vitro in a similar dose-dependent manner. In vivo, heparin treatment [continuous intravenous (i.v.) administration, 60 IU/h/kg body weight (0.35 mg/h/kg)] inhibited all aspects of the aortic reaction for < or = 28 days after injury: synthesis of DNA (early peak of thymidine incorporation into DNA on D3.5); accumulation of DNA, collagen and elastin on D14 and D28; intimal thickening on D14. An equivalent treatment with CY 216 [60 antiactivated factor X (Xa) IU/h/kg (0.71 mg/h/kg)] exerted similar though less intense effects on the reaction of intima-media, as assessed biochemically, but reduced formation of neointima in a proportion nearly identical to that of heparin. In some respects, which appear to be related mainly to the fibrotic reaction of aortic media to injury, heparin tended to be a slightly more potent antisclerotic agent than CY 216 although, owing to pharmacokinetic differences, CY 216 had stronger plasma anti-Xa activity than heparin.

Animals↗
PubMed1994

[Mechanisms of macrovascular involvement in diabetic subjects].

Diabetic macroangiopathy is often viewed as an accelerated and aggravated form of atherosclerosis. Several biological disturbances that are associated with diabetes partially account for a possible aggravation of atherosclerosis. Such are disorders of blood lipids (increased triglyceride concentration, modifications of low density lipoproteins) of haemostatis (increased platelet activity, decreased fibrinolytic activity) or of arterial vasomotility. Yet, many uncertainties and inconsistencies still obfuscate the links between diabetes and atherosclerosis, which remain hypothetical, and debatable. Clinical experience and all clinical epidemiological studies show that the incidence and severity of ischaemic arterial diseases (coronary heart disease, lower limb ischaemia, cerebral ischaemic events) are increased in diabetic individuals. However, intermediates other than worsened atherosclerosis may account for these associations. For instance, several anatomical epidemiological studies, based on routine autopsies, have note consistently found that atherosclerotic lesions (plaques) are larger and more extensive in diabetic than in non-diabetic individuals. The basic mechanisms of diabetic macroangiopathy could therefore be not as closely related to atherosclerosis as is usually thought. Among the non-atherosclerotic lesions that could explain the increased arterial risk in diabetic patients, the best documented and most plausible is arteriosclerosis--a pure sclerosis of the arterial wall (without lipid deposition) which, in its advanced forms, can compromise tissue vascularization. Arteriosclerosis is considered as a normal consequence of arterial ageing which would be accelerated in diabetes. Chronic hyperglycaemia is and independent and influent marker of arterial risk in diabetic patients. It could stimulate arterial sclerosis by enhancing non-enzymatic glycation of various components of the arterial matrix, through formation of advanced glycation end-products (AGEs).(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed1993

[Marine oils and prevention of cardiovascular diseases].

Observations done in Greenland Eskimos, and then confirmed in other populations, have led to the hypothesis that a diet rich in marine oils is associated with a low incidence of coronary heart disease. Marine oils are rich in n-3 polyunsaturated fatty acids which, if consumed in large amounts, influence plasma lipid concentrations (mainly by lowering triglycerides), and modify the synthesis of eicosanoids (leukotrienes and prostanoids) with effects on haemostasis, vasomotility and inflammation. Many experimental studies suggest that fish oils may exert and anti-atherosclerotic action. However, direct evidence (through prospective preventive trials) remains insufficient to establish that dietary supplements of marine oils prevent arterial diseases in humans efficiently. Aside from the treatment of hypertriglyceridaemia, no definitive recommendation can be made about the health benefits of marine oil supplement.

Cardiovascular Diseases↗