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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Platelet functions in relation to dietary fats in farmers from two regions of France. 42 66

The investigations were carried out in 30 patients with primary hyperlipidaemia (hypercholesterolaemia, hypertriglyceridaemia and mixed form). The serum total cholesterol and triglycerides, and in the erythrocytes the levels of AMP, ADP, ATP, ATP complex with Fe, MP, HDP and DGP were determined. Twenty blood donors served as a control group. The obtained results showed a statistically highly significant rise in ADP concentration in all investigated subgroups of hyperlipidaemic subjects, and a non-significant quantitative shift of other determined phosphate compounds.
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PMID:Certain phosphate compounds in the erythrocytes of patients with primary hyperlipidaemia. 50 54

Platelet aggregations stimulated with different concentrations of collagen or ADP were reduced during postprandial hyperlipemia in normolipemic subjects. The concomitant formation of platelet AA metabolites (TXB2, 12-HHT, 12-HETE), however, was not significantly altered.
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PMID:Postprandial hyperlipemia and platelet eicosanoid metabolism. 208 67

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.
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PMID:Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria. 261 81

The objective of this work was to characterize changes in platelet aggregability during postprandial hypertriglyceridemia with special emphasis on arachidonic acid metabolism. Ten healthy young men consumed 100 g fat after a fasting period of 12 hr. In-vitro platelet aggregation induced by ADP and collagen was measured at 0, 3, 5, and 9 hours after the fat intake. The major arachidonic acid metabolites, 12-hydroxyeicosatetraenoic acid (12-HETE), thromboxane A2 (TXA2), prostaglandin F2 alpha (PGF2a), and prostaglandin E2 (PGE2) produced during collagen-induced platelet activation were quantified by gas chromatography/mass spectrometry. A significant decrease in platelet aggregability induced by both ADP and collagen was detected during the postprandial hyperlipemia. No significant changes could be found in the prostanoid pattern of collagen activated platelets. There was no correlation between the degree of the inhibition of platelet aggregation and the relative or absolute increase of triglyceride-levels in the plasma during the postprandial hyperlipemia.
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PMID:Postprandial hyperlipemia inhibits platelet aggregation without affecting prostanoid metabolism. 130 85

The kinetics, in vivo distribution and sites of sequestration of autologous In-111-labelled platelets and other platelet function parameters were studied in ten patients with type IIa or IIb familial hypercholesterolaemia and thrombotic complications of atherosclerosis. The in vitro platelet aggregation response to ADP (P = 0.50) and collagen (P = 0.46); binding of fibrinogen to platelets (P = 0.61); and plasma beta-thromboglobulin levels (P = 0.42) of the patients and normal reference subjects did not differ significantly. The in vivo distribution of In-111-labelled platelets at equilibrium was within normal limits, and at the end of platelet life-span the sequestration pattern of labelled platelets in the reticuloendothelial system was also normal (spleen P = 0.31; liver P = 0.54). There was minimal evidence of in vivo platelet activation: only mean platelet lifespan (MPLS), 195 +/- 57 hours (difference between mean MPLS of patients and controls was 25 hours, with a 95% confidence interval from 23 to 31 hours; P = 0.02); mean platelet platelet turnover, 2298 +/- 824 platelets/microliter/hour (P = 0.005); plasma platelet factor 4 (P = 0.02); and the mean circulating platelet aggregate ratio, 0.8 +/- 0.1 (P = 0.02); differed significantly from normal. These results suggest that abnormalities of platelet function and kinetics observed in type II hyperlipoproteinaemia cannot be ascribed wholly to the hyperlipidaemia, but may be induced by the associated atherosclerosis.
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PMID:Kinetics and in vivo distribution of in-111-labelled platelets and platelet function in familial hypercholesterolaemia. 343 47

The influence of 2 different fatty meals, rich in either saturated or polyunsaturated fatty acids, on platelet aggregation in 7 normolipemic subjects and in 10 patients with phenotype IV hyperlipemia, was studied. 3 h after ingestion of a saturated- or polyunsaturated-fat-rich meal, plasma triglycerides were similarly increased in both groups. 5 h after ingestion of fat of either origin, the plasma triglyceride level in normal subjects returned almost to the fasting level, whereas in patients with hypertriglyceridemia it was still elevated. Platelet aggregation induced by ADP in platelet-rich plasma significantly increased in the normal group 3 h after both meals, whereas in the patient group it increased only after the saturated-fat-rich meal. These results were not changed 5 h after the meals. Postprandial elevated platelet activity was not correlated with increased plasma triglyceride concentration. No changes were found in washed-platelet aggregation in normal subjects, whereas the patient-derived washed platelets showed increased aggregation after the saturated-fat-rich meal. Plasma chylomicrons prepared from both groups during alimentary hyperlipemia inhibited ADP-induced platelet aggregation as well as thrombin-induced platelet 14C-serotonin release. This study indicates that the intake of fatty meals induces acute disturbance in platelet aggregation, favoring thrombosis. These changes are more comprehensive in hyperlipemic patients and after a saturated-fat-rich meal.
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PMID:Increased platelet aggregation during alimentary hyperlipemia in normal and hypertriglyceridemic subjects. 375 24

Platelet function and composition, lipemia, and dietary habits were evaluated yearly in 98 male farmers from Moselle (East of France) before and after decreasing, in half of them, dietary saturated fats from 16.2% to 9.9% of calories (P/S from 0.32 to 0.97). One year after these dietary changes, cholesterol and triglycerides decreased by approximately 10%, platelet aggregation to thrombin by 81%, and their clotting activity by 30%. However, ADP aggregation was enhanced by 54%. At 2 yr the P/S was decreased to 0.7 and diet also modified in controls, with 18:2 being increased mostly in one group (P/S = 0.81) and 18:3 in another (P/S = 0.59). In both groups, the main platelet function tests were significantly depressed 1 yr later. Considering the whole study, the intake of saturated fat was mostly correlated (group and individual) with platelet aggregation to thrombin, platelet clotting activity, and 20:3 (n-9) in plasma and platelet lipids.
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PMID:Influence of long-term diet modification on platelet function and composition in Moselle farmers. 394 87

This article reviews the experimental and clinical evidence regarding heparin therapy in the prophylaxis of coronary heart disease. The actions of heparin take place at the vascular endothelium where injected heparin concentrates, and within the bloodstream. At the endothelium heparin acts to prevent endothelial injury, prevent thrombin generation, prevent platelet adhesion to endothelium, and to decrease uptake of serum lipoproteins. Within the bloodstream heparin increases lipoprotein lipase activity and reduces the concentration of atherogenic very low-density lipoproteins. The reduction in lipemia enhances oxygen transfer from blood to the tissues, and decreases thrombin or ADP-induced platelet aggregation. Heparin increases the concentration of high-density lipoproteins. It decreases hypercoagulability and inhibits overactivation of serum complement. Heparin reduced atherosclerosis in most studies in cholesterol-fed animals. In human subjects who had a myocardial infarct at least one year before the onset of treatment, long-term intermittent heparin therapy significantly decreased cardiovascular deaths as compared to control groups.
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PMID:Heparin and atherosclerosis. A review of old and recent findings. 698 41

Effects of trapidil and other coronary vasodilators on retrograde blood flow in acute coronary-ligated dogs, isolated large and small coronary arteries of pig, platelet aggregation, biosynthesis of prostacyclin in isolated aortic rings and hyperlipemia in quails were investigated. Trapidil showed an increase in retrograde blood flow while dipyridamole, nifedipine, diltiazem and dilazep did not. Trapidil and nitroglycerin relaxed large coronary arteries, while dipyridamole, diltiazem, dilazep and adenosine relaxed small arteries. Trapidil, dipyridamole, diltiazem and aspirin protected against the secondary phase of ADP-induced platelet aggregation in guinea-pig platelet rich plasma more effectively than did nifedipine and dilazep. Trapidil and aspirin protected only against rabbit platelet aggregation as induced by arachidonic acid. Moreover, only trapidil protected against platelet aggregation as induced by prostaglandin G2-thromboxane A2 mixture. Trapidil and dipyridamole enhanced the platelet aggregation protection of prostacyclin. Trapidil also facilitated biosynthesis of prostacyclin more markedly than did the other drugs. Trapidil increased serum content of HDL cholesterol and significantly lowered serum content of triglyceride and the ratio of LDL cholesterol to HDL cholesterol in hyperlipemic quails. Dipyridamole, diltiazem, nifedipine and dilazep, however, showed little effect.
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PMID:[Pharmacological properties of trapidil: comparison with other coronary vasodilators (author's transl)]. 700 45


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