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C Léger

Publications and source records attributed to C Léger.

36 records · Page 2Linked to original sources
PubMed1974

Activation of Hageman factor and initiation of hepatic vein thrombosis in the hyperlipemic rat.

Hepatic vein thrombosis initiated by an intravenous injection of endotoxin (Salmonella typhosa, 0.3 mg/kg) resulted in an incidence of 78% in rats fed a butter-rich diet (group 1). On the other hand, no lesion could be produced in control animals fed corn oil (group 2) or standard chow (group 3). In regard to the respective thrombotic tendencies, the rats fed butter showed higher circulating levels of factor XII (175% vs 140% in group 2 and 100% in group 3) and a far more severe decrease in this factor (41% vs 15% in group 2 and 7% in group 3) and in platelets (48% vs 25% in group 2 and 19% in group 3) 2 hours after the injection of endotoxin. The triggering effect of endotoxin could be reproduced by ellagic acid, a known activator of factor XII. Given by slow infusion (1 mg/kg/min) this chemical induced hepatic vein thrombosis in 52% of the rats fed the butter-rich diet. Furthermore, inhibition of factor XII activation by lysozyme (20 mg/kg/min) completely prevented hepatic vein thrombosis initiated by endotoxin in butter-fed animals. It is concluded that, in addition to the potent hypercoagulability induced by the fat-rich diets, activation of Hageman factor consecutive to endotoxin injection is essential for production of the phenomenon of hepatic vein thrombosis.

Animals↗
PubMed1974

On the mechanisms responsible for selection of hepatic veins as target for thrombosis following injection of endotoxin in hyperlipemic rats.

The feeding of a butter-rich diet, to sensitize rats for studying the phenomenon of hepatic vein thrombosis, is shown to produce severe liver steatosis leading to a sinusoidal barrage and portal hypertension. The portal pressure in these animals was 210 +/- 4 mm of saline, as compared to 113 +/- 3 mm in the normal rat. Blood circulation studies using carbon suspensions revealed production of a vascular stasis in the hepatic veins after 60 to 90 minutes, when endotoxin (Salmonella typhosa, 0.3 mg/kg) is introduced into the blood circulation to initiate hepatic vein thrombosis. Similar results were observed after 15 minutes with ellagic acid (1 mg/kg/min). The stasis was found in connection with an additional intrahepatic resistance to blood flow as evidenced by a rise in portal pressure and by a reduction in liver perfusion in relation with development of systemic hypotension. In contrast with this, endotoxin initiated only slight and transient changes in the normal rat. Thrombosis immediately followed production of stasis in the hepatic vein, whether the phenomenon was initiated by endotoxin or ellagic acid. Furthermore, inhibition of the vascular stasis of alpha-adrenergic blockade (phenoxybenzamine, 3 mg/kg) was accompanied by prevention of hepatic vein thrombosis. It is concluded that stasis in the hepatic veins resulting from a mechanical obstruction of the circulation by steatosis and by an additional reduction in blood flow initiated by endotoxin, is responsible for selection of hepatic veins as targets for thrombosis following injection of endotoxin in hyperlipemic rats.

Animals↗
PubMedDate not supplied

Further results on lipase-colipase interactions studied by affinity chromatography.

Affinity chromatography of lipase on a colipase-coupled gel was studied in the present paper. The elution volume of the associable lipase increased when the loaded amount decreased. A KD value of 1.9 X 10(-6) M at pH 6.2 was thus deduced. A minimum value of 1.5 X 10(-6) M was obtained at pH 5.1-5.3. Mixed micelles associated with coupled colipase, but no modifications of lipase-colipase interactions took place when mixed micelles were added to the elution buffer. DMMA-modified coupled colipase failed to interact with lipase, owing to the specific orientation of the modified cofactor in the gel.

Animals↗
PubMedDate not supplied

[Vitamin E and cardiovascular prevention].

The antioxidant properties of vitamin E are well established. In humans, they appear very clearly from the nutritional supplementation trials. There is a strong correlation between supplied doses (>= 50 mg/j), vitamin E content of LDL and antioxidant protection of LDL. The consumption studies mostly suggest that the cardiovascular disease risk is diminished by the vitamin E supplementation, this being not true for vitamin E supplied by food strictly. In spite of the fact that there is a coherence between these results due in particular to the highly atherogenic role of oxidized low density lipoprotein, it is not allowed to claim that only the increased protection of LDL against oxidation is responsible for the diminished risk. The cell-regulating properties of vitamin E that have been more recently discovered have also to be taken into account as regards the functions of platelets, monocytes-macrophages, endothelial cells and vascular smooth muscle cells. The LDL-vitamin E capacity at decreasing the superoxide anion production (involved in turn in the oxidation process of LDL) could also play a role in preventing cardiovascular risk. The nutritional intervention studies undertaken in secondary prevention indicate a beneficial effect in terms of cardiovascular morbidity, either for low dose (50 mg), or for higher dose (>= 270 mg/d) intake, but without effect in terms of mortality. A recent study presumably supports a beneficial effect at the dose intake of 300 mg/d only in terms of cardiovascular mortality. Only one intervention has been carried out in condition of primary prevention, leading to the absence of effect at the dose employed (50 mg/d). The studies on the mechanisms of action make plausible the beneficial effects observed in analytical or experimental epidemiology. However, the experimental epidemiology does not provide indisputable evidence for the efficacy of the secondary prevention of cardiovascular risk by vitamin E supplementation. There is no intervention study using doses higher than 50 mg/d in primary prevention. There is a need for such studies in the not too distant future. A period of several years will be necessary before having new data possibly resulting in a consensus achievement.

Aged↗
PubMedDate not supplied

[Vitamins and aging].

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