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Biomedical subjects

S Renaud

Publications and source records attributed to S Renaud.

At least 109 records · Page 6Linked to original sources
PubMed1981

[Sleep states and oxymetry in neonates (author's transl)].

We have performed continuous recording of cutaneous PO2 (cPO2) together with a polygraphic recording of sleep in 12 normal premature babies, 36-38 weeks of post-conceptional age. In all babies, cPO2 was significantly lower (77.2 +/- 23.2) and more variable in active sleep than in quiet sleep (81.8 +/- 24.6). This difference is significantly related to the more numerous apneas, to the asynchronism of thoracic and abdominal movements, and to the motor activity with important irregularities of ventilation observed during the stage of active sleep.

Female↗
PubMed1980

[Influence of fenofibrate on blood platelet functions (author's transl)].

A study of blood lipids and platelet functions was conducted in north-eastern (Moselle) and southeastern (Var) France, among populations with widely different dietary habits and coronary disease mortality rates. Striking variations were found between the two populations with regard to platelet coagulation activity and response to various aggregation agents. On the other hand, plasma cholesterol, HDL-cholesterol and triglyceride levels were identical. Voluntary reduction by 53 subjects from Moselle in the consumption of saturated fats resulted, within one year, in remarkable improvement in platelet functions, thus demonstrating that the differences were due to diet and not to genetic factors. This being established, two studies were undertaken comparing healthy, normolipaemic subjects (control group) with two groups of type IIb hyperlipaemic subjects following the same pre-established diet and either untreated or treated with fenofibrate. They showed platelet hyperaggregation response to epinephrine in untreated subjects, whereas platelet functions in fenofibrate-treated subjects were identical with those in the control group. It would therefore seem that for many coronary disease patients changes in dietary habits combined with fenofibrate treatment might be one of the simplest and quickest ways of preventing the recurrence of myocardial infarction.

Blood Coagulation↗
PubMed1980

Biosynthesis of cholesterol and cholesterol precursors in platelets of female rats treated with oral contraceptives.

Rat platelets were incubated with sodium [U-14C]acetate and labeled lipids were analyzed. The major part of the radioactivity was found in phospholipids and in acylglycerols. When the incubation was performed with platelets of female rats treated with contraceptives, the total incorporation of labeled acetate in lipids was 2-fold higher and 33.6% of the radioactivity was found in lanosterol plus 24-dihydrolanosterol. Moreover, there is labeling of cholesterol. All these compounds were analyzed and identified by gas-liquid chromatography/mass spectrometry. In the incubation with sodium [2-14C]mevalonate the labeling of lanosterol plus 24-dihydrolanosterol and of cholesterol was increased by 30% in platelets of treated rats. The effect of contraceptives on one step of cholesterol biosynthesis is discussed and a possible explanation of the correlation between oral contraceptives and thromboembolic accidents is suggested.

Acetates↗
PubMed1980

Oral contraceptives, lanosterol, and platelet hyperactivity in rat.

Lanosterol, a cholesterol precursor that increases considerably in the platelets of rats treated with oral contraceptives, was incubated with either platelet-rich plasma or washed platelet suspension. After 2 minutes there was a remarkable dose-related increase in platelet activity. This platelet hyperactivity was measured by clotting time and platelet aggregation could not be reproduced by cholesterol or ethinylestradiol.

Animals↗
PubMed1980

Dietary fats and platelet function in French and Scottish farmers.

Although the intake of saturated facts still appears to be the environmental factor most closely associated with coronary heart disease (CHD), this does not necessarily mean that CHD is caused essentially or solely by blood lipids, as suggested by several investigators. It seems that blood platelets rather than (or at least in addition to) blood lipids might be the intermediate link between certain environmental factors (saturated fats, hard water) and CHD, through an effect on both thrombosis and atherosclerosis. Our recent studies in French and Scottish farmers, have shown that blood platelet function is more drastically affected by saturated fats than blood lipids. In those studies, platelet function was the only blood parameter correlated on an individual basis with the intake of saturated fat and inversely related to calcium intake. Calcium is probably the cation responsible for the protective effect of hard water against CHD in various countries. The results obtained also indicate that platelet function can be improved by increasing the intake of polyunsaturated fats at the expense of saturated fats. Finally, only platelet function was different from one region of France to another and from our region of Scotland to another; this difference could be related to the reported incidence of CHD in these various regions.

Adult↗
PubMed1980

[Essential fatty acids and the platelet membrane in relation to aggregation].

In man as in animals, the intake of long chain saturated fatty acids (14:0, 16:0, 18:0) representing 95% of the human diet saturated fatty acids, induce a similar increase in platelet functions (coagulation and aggregation to thrombin) to this found in coronary patients or subjects highly susceptible to coronary disease. These platelet function abnormalities resemble those observed in essential fatty acids deficient animals both being characterized, in the platelet phospholipids, by an increase in 18:1 and 20:3 omega 9, at the expense of the fatty acids from the omega 6 series. The platelet function and composition changes can be reversed by increasing the dietary intake of 18:2, a specific effect (at least for polyunsaturated fatty acids) since it cannot be reproduced by a monoeme such as oleic acid.

Animals↗
PubMed1980

A comparison of the effects of dietary short and long chain saturated fatty acids on platelet functions, platelet phospholipids, and blood coagulation in rats.

Rats were fed for 20 weeks balanced purified diets solely enriched in fat, to determine whether, as in diets containing cholesterol and cholic acid, it was mostly the common dietary long chain saturated fatty acids (16:0 and 18:0) which could induce platelet function abnormalities. The dietary fats rich in 16:0 and 18:0 induced increased thrombin and adenosine diphosphate (ADP) platelet aggregation and an acceleration of the platelet-rich plasma clotting time. These effects on platelet functions were coupled with increased levels of 20:3 omega 6 and 20:3 omega 9 in total platelet phospholipids and a decrease of 22:4 and 24:4 omega 6 in the platelet phosphatidyl ethanolamine. Fatty acids that most closely correlated with thrombin aggregation and plasma clotting time (r = 0.99) were 20:3 omega 9 and 22:4 omega 6. There was no relationship between the effects of dietary fats on blood lipids and on blood platelets. Consequently, in different experimental models in rats, the dietary long chain saturated fatty acids appear to be responsible for certain platelet function abnormalities (clotting activity, response to thrombin aggregation). These platelet abnormalities might be due to changes in the platelet phospholipid fatty acid composition.

Adenosine Diphosphate↗
PubMed1979

Platelet functions in relation to dietary fats in farmers from two regions of France.

To determine whether the long-term feeding of dietary fats affect platelet functions in man, platelet aggregation (to thrombin ADP, collagen, epinephrine) and clotting activity of platelet-rich plasma (PRP), platelet-poor plasma and of washed platelets were studied in a mobile-laboratory in 44 healthy male farmers (40--45 years) from two French regions Var and Moselle, in relation to lipemia, glycemia, dietary nutriments, and platelet phospholipid composition. In the Moselle subjects, the platelet clotting activity of PRP and of washed platelets, the platelet aggregation to thrombin and ADP, were highly significantly (p less than 0.001) increased as compared to those of Var, but not the plasma cholesterol, which was identical in the two regions. In Moselle, the intake of total calories, total lipids and saturated fats was higher than in the Var. However, it was only with the saturated fat intake (mostly stearic acid) that the platelet clotting activity (p less than 0.01) and the platelet aggregation (p less than 0.001) were highly significantly correlated. The platelet clotting activity was also significantly (p less than 0.001) correlated with the fatty acid composition of the platelet phospholipid fractions phosphatidyl serine + phosphatidyl inositol.

Adenosine Diphosphate↗
PubMed1979

Modification by oral contraceptives in rat of 14C acetate incorporation into platelet lipids.

The in vitro incorporation of acetate 14C in platelets lipids was compared in control female rats (Gr. I) to rats treated for 4 days either by an oral contraceptive ethinyl oestradiol + lynestrenol (Gr. II), or by ethinyl oestradiol alone (Gr. III) or lynestrenol alone (Gr. IV). An increase of 43--45% in the incorporation of acetate could be observed in the two groups (II and III) which received ethinyl oestradiol, while the incorporation in group IV was similar to that of the controls. The lipid fractions of which the synthesis was the most considerably stimulated by the oestrogen treatment, were the neutral lipids as separated from the other lipids by TLC. In groups II and III the incorporation in cholesterol and cholesterol esters was increased by 8 fold and by 10 fold in the free fatty acid fraction. In these two groups, even in the phospholipid fractions PS + PI and PE, the radioactivity was significantly increased. The observed effect of the oral contraceptive studied here on platelet lipid synthesis in female rats, appears to be essentially due to the estrogens, since lynestrenol had only minimal effects in that respect.

Acetates↗
PubMed1979

Influence of a hypolipemic drug (procetofene) on platelet functions and lipid composition in type II B hyperlipoproteinemia.

Platelet function was evaluated in platelet-rich plasma and in washed platelets in relation to their lipid composition, in 18 type II B hyperlipoproteinemic men treated with procetofene. The results were compared to those obtained in 15 young, healthy normolipemic controls and in 22 untreated male subjects with type II B hyperlipoproteinemia. In addition to completely normalizing platelet functions, procetofene was able to induce a 28-53% decrease in serum cholesterol and triglycerides. Solely, the aggregation to ADP (secondary), arachidonic acid and epinephrine was higher in the untreated hyperlipoproteinemic subjects. This increased susceptibility to aggregation does not appear to be related to the cholesterol or cholesterol-phospholipid content of platelets.

Adenosine Diphosphate↗
PubMed1979

Dietary fats and platelet functions in relation to atherosclerosis and coronary heart disease.

Results in animals and in man indicate that in many circumstances, lipemia is not closely related to the severity of atherosclerosis nor to the incidence of coronary heart disease (CHD) or the intake of saturated fats as observed in paired studies between farmers from Moselle and Var in France and from West and East Scotland. In rabbits, an increased response of platelets to thrombin occurs before any deposition of cholesterol, as a result of a saturated fat feeding. Under these conditions, the addition of alcohol to the drinking water decreases significantly both the platelet response to thrombin and the severity of atherosclerotic lesions without much affecting plasma cholesterol. In farmers from Moselle and Var (as well as from Scotland), platelet functions, namely the aggregation to thrombin and their clotting activity, i.e. PF3, are closely related to the intake of saturated fats, either as a result of the long-term feeding or of a 1 year change in the diet of Moselle farmers. Certain platelet functions appear to be the only blood parameter related to the incidence of CHD and significantly correlated on a group, as well as on an individual basis, with the intake of saturated fat, and inversely related with that of calcium. Saturated fats and calcium are known to be the two main dietary factors related to CHD. These results suggest that the intermediate link between dietary fats and CHD might be blood platelets rather than serum lipids, through an effect on both thrombosis and atherosclerosis.

Alcohol Drinking↗
PubMed1976

[Thrombogenic and atherogenic effects of dietary fats].

1. Epidemiologic studies have shown that CHD (arterial thrombosis) and venous thrombosis were closely associated with dietary saturated fat intake. 2. In vitro and in vivo studies are unanimous in that long chain saturated fatty acids, mostly-stearic acid, are thrombogenic, while linoleic acid has protective effects. 3. Stearic acid appears to modify the fatty acid composition of platelet phospholipids resulting in an increase in the aggregating and clotting capacities of platelets. 4. In coronary patients or in subjects eating saturated fats, similar modifications in platelet behaviour can be observed related to changes in platelet phospholipids. Those results appear to confirm the hypothesis that certain dietary saturated fats, in addition to induce hyperlipemia and atherosclerosis, predispose to thrombosis mostly through blood platelets.

Adult↗