Search PubMed⌕ Search

Biomedical subjects

L Capron

Publications and source records attributed to L Capron.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1984

[Epidemiology and risk factors of cerebral arterial accidents].

In France, available epidemiologic data (mortality statistics, Paris prospective study)--although still insufficient--indicate: 1) that arterial strokes account for about 13 per cent of all deaths, and 2) that their annual incidence in men aged 40 to 60 is around 0.6 per thousand and increases sharply thereafter. These results are comparable to those of other industrialized countries, with the exception of Japan where the actual incidence of arterial strokes seems to be higher. Age and high blood pressure are the major risk factors and causes of the various types of ischaemic and haemorrhagic arterial strokes. Several studies suggest that the treatment of hypertension significantly decreases the incidence of arterial strokes.

Adult↗
PubMed1984

Diabetes and insulin: actions and interactions upon the glucose metabolism of rat aorta.

We studied the glucose oxidation to CO2 and the incorporation of glucose into lipids by thoracic aorta from streptozotocin-diabetic rats in two circumstances: 9 minutes exposure of the isolated aorta to insulin, perfused in situ; and one-week treatment with either low--4 units (U)--or high--12 U--daily doses of insulin. Diabetes inhibited the glucose metabolism of media and adventitia. Perfusion with insulin did not influence the depressed metabolism of media but increased that of adventitia. Four units insulin treatment normalized the synthesis of glucose-derived lipids by the media, whereas 12-U treatment brought it to levels significantly higher (+23%) than those found in nondiabetic rats. We conclude that: (a) a haemodynamic explanation cannot account for the in vitro insulin resistance of media found in diabetes; (b) insulin treatment exerts a dose-dependent lipogenic effect upon the media, which might favour an atherogenic role for therapeutic hyperinsulinaemia in insulin-dependent diabetics.

Animals↗
PubMed1983

[Atherosclerosis. Description and mechanisms. Part 1: description].

This review is devoted to the cellular biology of the arterial wall, particularly of the cerebral arteries. Starting with the description of the structure and physiology of normal arteries and of atherosclerotic lesions some of the current theories on the mechanisms of atherosclerosis are considered. They have developed along two lines of thinking according to whether the main role is given to arterial smooth muscle cells or to macrophage cells. Both hypotheses view atherosclerosis as a pathological deviation from a physiological reaction aimed at maintaining and repairing the permanently strained arterial intima. The risk factors, as identified by epidemiological studies, are likely to play a major role in this degenerative process.

Arteries↗