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Biomedical subjects

L Capron

Publications and source records attributed to L Capron.

At least 73 records · Page 4Linked to original sources
PubMed1988

[New concepts of atherogenesis].

The main advances since 1980 in our understanding of atherosclerosis can be summarised under four headings. 1) The migration and proliferation of smooth muscle cells from the media into the intima are key-events of atherogenesis, and probably also of restenosis following percutaneous transluminal coronary angioplasty. The experimental study of their regulations, especially looking for inhibitors, has therefore gained increased interest as it may provide original approaches to the prevention of post-angioplasty restenosis. 2) The histiocytes/macrophages, derived from blood monocytes, also take a major part in the initiation of atherosclerotic lesions. An intensive research activity is now being devoted to elucidating the many facets of their participation in atherogenesis. 3) Brown and Goldstein's discoveries have explained the biochemical mechanisms of the increased plasma low-density lipoprotein (LDL) concentration found in familial hypercholesterolemia (type IIa), although they did not completely solve the enigma of lipid deposition in the arterial wall. The metabolic handling of modified LDLs appears to be crucial to the foamy transformation of macrophages and, possibly, of smooth muscle cells. 4) Risk factors identified by epidemiology are usually held responsible for atherosclerosis. Yet this causal interpretation is not entirely satisfactory, and alternative or complementary hypotheses are being but forward. Among them, the most consistent submits that a viral aggression of the arterial wall is involved in the genesis and progression of atherosclerosis.

Angioplasty, Balloon↗
PubMed1988

Association of inherited dysfibrinogenaemia and protein C deficiency in two unrelated families.

An inherited association of dysfibrinogenaemia and protein C deficiency was found in three members of the same family. The propositus was a 48-year-old man who suffered from severe and rapidly complicated atherosclerosis of the aorta and lower limbs arteries, which perhaps suggests that the association of these two molecular abnormalities may have enhanced the thrombotic process. The abnormal fibrinogen had a reduced ability to bind thrombin which may be thrombogenic. We found the same inherited association of dysfibrinogenaemia and protein C deficiency in a patient with venous thrombosis. The functional abnormality of the fibrinogen, which could have been responsible for thrombosis, was delayed proteolysis by plasmin. Not only fibrinogen, but also fibrin clots were resistant to plasmic degradation. These observations raise two questions: (1) Is the association of a protein C deficiency with a dysfibrinogenaemia fortuitous or the result of a common mechanism? (2) Is there a link between an increased thrombotic tendency and either both of the defects of haemostasis that we have found, or only one of them?

Adult↗
PubMed1987

Antithrombin III and heparin cofactor II in patients with chronic renal failure undergoing regular hemodialysis.

Heparin enhances the inhibition rate of thrombin by both antithrombin III (AT III) and heparin cofactor II (HC II). We studied the activity of these two plasma proteins in patients with chronic renal failure (CRF) undergoing regular hemodialysis as their heparin requirements varied widely. In 77 normal blood donors, normal ranges (mean +/- 2 SD) were 82-122% for AT III and 65-145% for HC II. When compared with these controls 82 dialyzed CRF patients had a subnormal AT III activity and a significantly (p less than 0.001) lower HC II activity. To evaluate the effect of hemodialysis we compared AT III, HC II and total proteins in plasma before and after dialysis in 24 patients (12 with normal and 12 with low basal HC II activity). AT III and HC II activities significantly (p less than 0.001) increased in absolute value. When related to total plasma proteins, in order to suppress the influence of hemoconcentration induced by dialysis, AT III decreased significantly (p less than 0.01) whereas HC II increased slightly but significantly (p less than 0.01) in the 12 patients with low initial HC II activity. The decrease of AT III induced by heparin administrated during dialysis is likely to account for this relative decrease of AT III activity. A modification of the distribution of both HC II and heparin between the vascular wall and the circulating blood is evoked to explain the relative increase in HC II activity and the need for higher heparin dosage in patients with low HC II levels.

Adult↗
PubMed1987

An abnormal antithrombin III (AT III) with low heparin affinity: AT III Clichy.

We have identified an inherited qualitative deficiency of antithrombin III (AT III) in a family with apparently no increased incidence of venous thrombosis. Plasma antithrombin and anti-Xa activities were normal, but the interaction with heparin, heparan sulphate and low molecular weight heparin was uniformly decreased. An immunoblotting technique performed in plasma showed normal complex formation with thrombin. By using heparin-Sepharose affinity chromatography and crossed immunoelectrophoresis, the variant could be separated: at least two fractions of low affinity AT III were obtained. A minor one had no antiprotease activity; the other one was further purified to homogeneity and found to have normal specific activity in absence of heparin and a 50% decreased activity in presence of heparin. We propose to call this new variant AT III Clichy.

Adult↗
PubMed1987

Effects of insulin and hydrostatic forces on the metabolism of the aorta.

To better understand the putative association between insulin and atherosclerosis many experimental studies have explored the metabolic effects of insulin upon the arterial intima-media (which is essentially made up of smooth muscle cells). This tissue appears to be insulin-sensitive in vivo but not in vitro, suggesting that the actions of insulin on arterial metabolism are probably indirect. Yet, cultured arterial smooth muscle cells do increase their anabolism when physiological concentrations of insulin (10-250 microU/ml) are added to the medium. To account for these discrepancies we have proposed a haemodynamic explanation : hydrostatic forces present in vivo but absent in vitro, would be necessary for insulin to reach the cells of the media and act upon them. We demonstrated such an effect using an isolated rat aorta perfused under variable pressure. But only highly unphysiological concentrations of insulin (0.1 mU/ml) could stimulate the metabolism of intima-media significantly. The insulin-sensitivity of the target tissue for atherosclerosis remains an enigma. We speculate that the variable phenotype of arterial smooth muscle cells (either contractile or synthetic) might be an interesting clue to this problem.

Animals↗
PubMed1986

Growth-promoting effects of diabetes and insulin on arteries. An in vivo study of rat aorta.

Proliferation of arterial smooth muscle cells is regarded as an important event in atherogenesis, which according to in vitro culture studies is influenced by diabetes and insulin. To assess whether this holds true in vivo, we studied the cellular kinetics of thoracic aorta in normal and streptozocin-induced diabetic rats with and without insulin treatment. We measured the incorporation of [3H]thymidine into intima-media, as well as its DNA content, 2 and 14 days after endothelial denudation. We found that the mitotic response of an injured artery is not modified by diabetes but is depressed by insulin treatment in nondiabetic rats, probably due to hypoglycemia. Our data in insulin-treated diabetic rats support but do not definitely settle the view that insulin is mitogenic as long as the treatment does not cause sustained hypoglycemia.

Animals↗