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Biomedical subjects

L Capron

Publications and source records attributed to L Capron.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1993

[Staphylococcus aureus endocarditis: an unusual clinical picture].

We describe an unusual presentation of bacterial endocarditis due to Staphylococcus aureus in a 50 year-old woman with mitral insufficiency. The disease began by a vascular purpura without fever and a digital embolism. The source of infection was anal ulcerations. Diagnosis of endocarditis was made possible by trans-oesophagus echocardiography but not by trans-thoracic echocardiography. The patient was successfully treated by surgery associated with antibiotherapy. This observation emphasizes the indications of surgery at the acute phase of endocarditis. The anal source of endocarditis is original, no other case has been found in the literature.

Echocardiography, Transesophageal↗
PubMed1993

[Immunity, inflammation and atherosclerosis].

Atherosclerotic plaques harbour 3 main cell types: arterial smooth muscle cells, monocyte-macrophages and T-lymphocytes. Together with other morphological characteristics, this feature concurs to the view that plaques are foci of chronic inflammation. The presence of T-cells suggests that immune mechanisms are involved in the development of atherosclerosis. Clinical studies have found correlations between the presence or progression of carotid plaques and the serum concentration of antibodies against oxidized low-density lipoproteins and against heat shock protein HSP-65. Along with other observations, these correlations, if confirmed and extended, may open new avenues to understand the triggering mechanisms of atherosclerosis. However, the available evidence is still insufficient to establish that an autoimmune involvement is a cause rather than a consequence of atherosclerosis.

Arteriosclerosis↗
PubMed1993

[Inflammatory mechanisms of atherosclerosis: pathogenic and etiologic inferences].

Inflammation is the reaction of a vascularized living tissue to local injury. At its chronic stage, inflammation displays 4 characteristic features that are all to be found in atherosclerotic plaques: lympho-monocytic infiltration; sclerosis; cellular proliferation; vascular proliferation. This view sheds new light and opens new avenues for research on atherosclerosis. That is true for pathogenesis which progressively integrates the mass of information that has accumulated about the cellular and molecular mechanisms of inflammation. That is also true fort the aetiology of atherosclerosis where the causal enigmas are approached with a more open mind, much wider than the traditional concepts of degeneration and overloading that have prevailed for so long. In the near future, some promising therapeutic clues should derive from this renewed approach of atherosclerosis.

Arteriosclerosis↗
PubMed1992

Partial characterization of an autoantibody recognizing the secondary binding site(s) of thrombin in a patient with recurrent spontaneous arterial thrombosis.

A patient with an 18 year history of recurrent arterial thrombosis and no evidence of atherosclerosis or embolism of cardiac origin presented with a prolonged thrombin clotting time when performed with human thrombin. The bovine thrombin clotting time was only slightly prolonged. During 30 months of follow-up, the thrombin time fluctuated, but remained prolonged. The patient has been treated with an oral anticoagulant for the past 8 years, with no thrombotic recurrence. The inhibitor activity was due to the presence of polyclonal IgGs which bound to thrombin-Sepharose. The influence of IgGs purified from the patient's serum was compared to the influence of normal IgGs in several systems exploring the catalytic activity of thrombin and the binding of the enzyme to macromolecular substrates through secondary binding site(s). We found that the IgGs did not impair the catalytic activity toward small synthetic substrates, but inhibited the binding of thrombin to fibrinogen, thrombomodulin and heparin cofactor II. Such proteins are known to require a secondary binding site of thrombin to interact with the enzyme. The anti-thrombin antibody might have resulted from an abnormal generation of thrombin. This would be the consequence of the process favouring thrombosis. Alternatively, the autoantibody might have favoured thrombosis primarily, by impairing natural antithrombotic mechanisms triggered by thrombin.

Adult↗
PubMed1992

In vivo proliferation of rat vascular smooth muscle in relation to diabetes mellitus insulin-like growth factor I and insulin.

The roles of diabetes mellitus, insulin-like growth factor I and insulin in vascular smooth muscle proliferation in vivo were studied. Proliferation was induced by endothelial injury (balloon catheterization) of rat aorta, and was measured as 3H-thymidine incorporation into DNA. Levels of insulin-like growth factor I mRNA and insulin-like growth factor I receptor mRNA were measured with a solution hybridization assay. The increase in DNA synthesis was most pronounced 2 days after injury in both normal and diabetic rats and declined thereafter, but DNA synthesis in aortas from diabetic rats was lower throughout the time period studied. Levels of insulin-like growth factor I mRNA and the receptor mRNA were both increased in balloon catheterized aortas, and time-course studies showed an increase in receptor mRNA prior to the increase in insulin-like growth factor I mRNA. Diabetic rats were treated with equimolar concentrations of insulin (35 nmol/day) or insulin-like growth factor I (31 nmol/day) for 5 days. Insulin-like growth factor I increased DNA synthesis in injured aortas 2 days after injury without improving blood glucose, whereas the effect of insulin was associated with a decrease in blood glucose levels. In conclusion, vascular smooth muscle proliferation is impaired by diabetes and stimulated by insulin treatment. Insulin-like growth factor I infusion stimulates vascular smooth muscle proliferation without affecting blood glucose, and gene expressions of insulin-like growth factor I and its receptor are increased in proliferating vascular smooth muscle, indicating that insulin-like growth factor I and involved in vascular smooth muscle proliferation in vivo.

Animals↗
PubMed1992

In vivo effect of insulin on the acute proliferative response of the rat aorta to injury.

The objective of our study was to investigate the effect of hyperinsulinemia associated with either euglycemia, hypoglycemia, or hyperglycemia on the short-term mitotic activity of arterial smooth muscle cells (SMCs) after aortic injury. The proliferative reaction of arterial SMCs was provoked by the passage of an embolectomy catheter with a tightly inflated balloon. DNA synthesis was measured as DNA specific activity after incubation of the aorta in a medium containing 3[H]thymidine. Unrestrained rats were rendered hyperinsulinemic (4-7 nM versus 0.3 nM in controls) immediately after aortic injury by insulin infusion (10 units/day) and either euglycemic (about 5.6 mM), hyperglycemic (14-17 mM), or hypoglycemic (about 2.8 mM) by adjusting the flow rate of hypertonic glucose (30% wt/vol) that was infused simultaneously. The infusion was performed via a catheter inserted into the jugular vein and lasted 2 or 4 days after the aortic injury. After the injury, SMC mitotic activity was dramatically increased on day 2 in control rats with deendothelialized aortas and declined between days 2 and 4. In euglycemic-hyperinsulinemic and hyperglycemic-hyperinsulinemic rats, SMC proliferation showed the same pattern as in controls. At no time was a significant difference observed among the three groups of rats. In hypoglycemic-hyperinsulinemic rats, SMC mitotic activity increased to a lesser extent than in controls on day 2 after deendothelialization. These data indicate that hyperinsulinemia with or without hyperglycemia does not stimulate the early stages of arterial SMC proliferation in the rat although a long-lasting effect of hyperinsulinemia cannot be excluded.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of ramipril, an inhibitor of angiotensin converting enzyme, on the response of rat thoracic aorta to injury with a balloon catheter.

We have studied the effect of ramipril (10 mg/kg daily by gastric gavage) on the development of neointima 2 and 14 days after injury to rat aorta with a balloon catheter. In treated animals, there was no significant inhibition of the early mitotic reaction after injury (synthesis of DNA, as reflected by aortic thymidine incorporation on the second day): the mean (95% confidence interval) was 3,553 (892) in the control group vs. 2,853 disintegrations/min/micrograms of DNA (555) in the treated group, 2 p greater than 0.15. However, ramipril decreased the amount of neointima formed 14 days after injury, as characterized by (a) a highly significant decrease of the intima to intima + media areas ratio [21.1 (2.4) vs. 13.7% (2.2), 2 p less than 10(-4]); (b) a significant decrease of intima-media wet weight [35.4 (1.0) vs. 30.9 mg (0.9), 2p less than 0.005]; and (c) without any significant effect on intima-media DNA content [96.3 (7.9) vs. 91.7 micrograms (5.7), 2p greater than 0.3]. These observations suggest that angiotensin converting enzyme inhibitors may not act mainly through an inhibition of smooth muscle cell proliferation. Other effects, such as inhibition of migration, hypertrophy, and matrix synthesis, should also be considered.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Effects of fasting and refeeding on the proliferative response of rat aorta to injury.

To explore the interplay between the mitotic activity of arterial smooth muscle cells and the variations of plasma glucose and insulin concentrations, we have studied over 14 days the response of thoracic aorta to injury with a balloon catheter in rats submitted to fasting and refeeding. Animals were fasted from the day before until the third day after injury. The proliferative reaction of intima-media was assessed 2, 3.5, 4, 6, 8, and 14 days after injury, comparing freely fed with fasted-refed rats. Fasting decreased plasma glucose and insulin concentrations and DNA synthesis by intima-media, whereas refeeding increased these three variables transiently. The DNA content of intima-media at any time during the response to injury and the intimal thickening on day 14 were not influenced by the sequence of fasting and refeeding, which suggests that the early decrease in DNA synthesis induced by fasting had been compensated for by the later increase in DNA synthesis induced by refeeding. In conclusion, besides hormonal influences (such as insulin), metabolic influences (such as the availability of energetic fuels) are likely to act on the proliferative response of arteries to injury.

Animals↗