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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ranges for near-threshold ADP concentrations for the aggregation of macaque and human citrated platelets overlapped. The minimum concentrations of epinephrine, 0.05 microM to 1.0 microM, that at least doubled the aggregation response at threshold ADP concentrations were comparable for macaque and human citrated platelets. Epinephrine (1.0 microM to 10 mM) alone never aggregated macaque citrated platelets. Biphasic aggregation occurred with both macaque and human citrated platelets. The addition of heparin to a final concentration of 2.2 units/ml had no effect on the threshold ADP concentrations or the sensitivity of macaque or human citrated platelets to epinephrine. One microM phentolamine eliminated the potentiating effect of 1 microM epinephrine on ADP-induced aggregation of macaque and human citrated platelets. The threshold concentrations of ADP for macaque platelets were sharply reduced when heparin was used as an anticoagulant rather than citrate. However, epinephrine induced a similar increase in aggregability with both citrated and heparinized platelets, 0.55 +/- 0.09 SEM% and 0.44 +/- 0.09 SEM%, respectively. These data indicate that macaque and human platelets behave in a similar manner in response to ADP and that epinephrine potentiates the ADP-induced aggregation of macaque and human platelets equally well.
Atherosclerosis 1986 May
PMID:Effects of ADP and epinephrine on macaque and human platelets. Implications for studies on human atherosclerosis. 371 10

Elevated plasma lipid concentrations and increased platelet activation are risk factors in the development of atherosclerosis. Nine patients with type IIa hyperlipoproteinemia and nine patients with type IV hyperlipoproteinemia were given soya lecithin, 12 g/day, for 3 months. Plasma cholesterol and triglycerides were reduced by 15 and 23%, respectively, and HDL-cholesterol increased by 16% in the hypercholesterolemic patients. Platelet function was unchanged. In the hypertriglyceridemic patients, total cholesterol fell by 18%, triglycerides by 36%, and HDL-cholesterol increased by 14%. There was a 27% reduction in platelet aggregation (P less than 0.01). Seventeen hypertriglyceridemic patients then received increasing doses of soya lecithin for 1-month periods (6, 12, and 18 g/day). The optimal lipoprotein-lowering effect was achieved with a daily dose of 12 g soya lecithin per day. Both low-density lipoprotein and very-low-density lipoprotein levels were reduced, and HDL-cholesterol and apolipoprotein levels were reduced, and HDL-cholesterol and apolipoprotein A-I concentrations were increased. Platelet aggregation in response to collagen and ADP was significantly reduced, parallel with the reduction in triglyceride level. Soya lecithin supplementing the diet may be useful in the management of the hypertriglyceridemic patient.
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PMID:Dietary soya lecithin decreases plasma triglyceride levels and inhibits collagen- and ADP-induced platelet aggregation. 377 75

Ca++ level in the platelets of patients with different forms of CHD (angina pectoris of new onset, including the spastic form, acute myocardial infarction) and of subjects without signs of CHD or coronary atherosclerosis was measured basally and after stimulation with ADP, platelet activation factor and serotonin. Simultaneously platelet aggregation induced by the same stimuli was studied. Basal platelet Ca++ did not differ significantly between the groups. Stimulation by ADP and serotonin increased Ca++ concentration, the change being greatest in patients with spastic angina pectoris. Augmentation of free platelet Ca++ in patients with acute myocardial infarction did not differ from that in subjects without CHD and coronary atherosclerosis, and in some cases it was even less pronounced. Free Ca++ level showed good correlation with platelet aggregation. It is suggested that the differences revealed are due to changes in the sensitivity of platelet receptors to the inductors used.
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PMID:[Free cytoplasmic calcium and thrombocyte aggregation in patients with ischemic heart disease. The effect of ADP, thrombocyte activation factor and serotonin]. 380 Nov 47

The objective of this study was to characterize and standardize whole blood electrical aggregometry (WBEA) in the pig and rabbit, animal models extensively used in atherosclerosis research, and to compare their platelet response with that of man. Platelet aggregation was studied in blood (WBEA) and platelet rich plasma (optical aggregometry, OA). Dose response curves were obtained for ADP and collagen. The effect of hematocrit on WBEA was also evaluated. Aggregation with ADP and collagen using WBEA was more extensive with human than with pig or rabbit platelets. OA revealed similar differences among species but the time to reach maximal aggregation was markedly shorter. Using WBEA, the extent of aggregation was inversely related to the hematocrit. We conclude that WBEA is a useful technique that may be of particular importance in situations where hyperlipidemic plasma prevents the use of OA, as occurs in some atherosclerosis research animal models.
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PMID:Electrical aggregometry in whole blood from human, pig and rabbit. 381 May 51

Feeding natural fats varying in contents of palmitate (16:0), stearate (18:0), oleate (18:1), and linoleate (18:2) to rabbits resulted in modulation of platelet phospholipid fatty acyl composition. Rabbits were fed high fat semipurified diets containing 2% corn oil (CO) + 18% CO, cocoa butter (CB) or milkfat (M) for periods of up to 300 d. Platelet phospholipid linoleate contents corresponded to diet levels with 18:2 highest in CO-fed rabbits and following the sequence CO greater than CB greater than M. Stearate was highest in CB-fed rabbits, corresponding to high 18:0 levels in CB, but palmitate levels were not affected by diet. Both CB and M-fed rabbits were higher than CO-fed rabbits in oleate. Though CO is highest in 18:2, the accepted 20:4 precursor, arachidonate was highest in M-fed rabbits. Adding cholesterol (0.2%) to the diets did not affect platelet phospholipid fatty acyl composition except to elevate 20:4 in M-fed rabbits. CO-fed rabbits showed uniquely high levels of tetracosadienoate (24:2). Fatty acyl composition data were essentially constant between 200 and 300 d on diet. Phospholipid fatty acyl unsaturation was apparently homeostatically controlled as mole percent unsaturate to saturate ratios were independent of diet. The observed homeostasis resulted in minimal diet influences on platelet membrane fluidity and ADP or collagen stimulated platelet aggregation. Platelet fluidity, determined by fluorescence polarization, was a function of oleate and linoleate contents of the cells. Cholesterol feeding generally lowered platelet fluidity and altered the dependence of fluidity on fatty acyl composition.
Atherosclerosis 1987 Jan
PMID:Influence of saturated and unsaturated fats on platelet fatty acids in cholesterol-fed rabbits. 382 74

In order to further characterize the modulation of the ADP-induced aggregation of gel-filtered human platelets by beta 2-glycoprotein-I (beta 2-G-I), the influence of this glycoprotein upon the serotonin (5-HT) release during aggregation was measured. The following results were obtained: beta 2-G-I completely inhibits the 5-HT release during ADP-induced platelet activation. The inhibition is correlated with the inhibition of the second wave of the ADP-induced aggregation. This effect of beta 2-G-I is not dose-dependent and appears above a threshold concentration of 0.1-0.15 mg/ml in the assay. The specificity of the beta 2-G-I interaction with the ADP-activation is supported by results obtained with collagen or thrombin as aggregating agents. In these cases neither the aggregation nor the release is influenced by the glycoprotein. In respect to the results obtained, beta 2-G-I is a potent candidate to be a modulator of ADP-induced platelet activation in vivo.
Atherosclerosis 1987 Feb
PMID:Beta 2-glycoprotein-I (apo-H) inhibits the release reaction of human platelets during ADP-induced aggregation. 382 75

Platelets from patients with familial hypercholesterolemia (type IIa hyperlipoproteinemia), a condition associated with a high prevalence of atherosclerosis and its ischemic complications, are claimed to be hyperresponsive to aggregating stimuli. We investigated the platelet responsiveness to and the binding of PGD2, a potent endogenous inhibitor of platelet aggregation via stimulation of adenylate cyclase, in a group of 7 patients affected by IIa hyperlipoproteinemia (IIa HLP) and in a control group of 10 healthy subjects. Inhibition by PGD2 of ADP-induced platelet aggregation was significantly lower in IIa HLP patients than in controls. The number of binding sites for PGD2 of platelets from IIa HLP patients was significantly reduced in comparison with that from controls (93 +/- 19 and 232 +/- 23 receptors/platelet, respectively), whereas the affinity for PGD2 was comparable to that of controls (Kd = 68.8 +/- 19.8 nM in patients and 66.1 +/- 15.9 nM in controls). The reduced number of platelet PGD2 binding sites in IIa HLP patients may account for the impaired sensitivity to PGD2 shown in vitro by platelets and may contribute to the increased tendency to thrombotic manifestations observed in IIa HLP.
Atherosclerosis 1985 Feb
PMID:Decreased number of PGD2 binding sites on platelets from patients with type IIa hyperlipoproteinemia. 385 47

The content of cholesterol in red cell and platelet membranes was lowered in rabbits with experimental atherosclerosis after intravenous injection of positively charged micelles of soybean phosphatidylcholine. That lowering was accompanied by a reduction in membrane microviscosity, rise of the activity of Na,K- and Ca-ATPases of red cells, and a decrease in the rate of the ADP- and collagen-induced platelet aggregation. Injection of phosphatidylcholine gave rise to an increase in the blood serum content of phospholipids and cholesterol in high density lipoprotein fractions, to a reduction in the content of triglycerides and the atherogenicity index, as well as to the lowering of the microviscosity of high density lipoproteins. The aortal area affected by atherosclerotic lesions was 2 times less in the group of animals given phosphatidylcholine.
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PMID:[Extraction of cholesterol from biological membranes with positively charged micelles of phosphatidylcholine]. 397 Oct 35

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.
Atherosclerosis 1985 Apr
PMID:The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid. 400 83

The release and the local activity of plasminogen activator (PA) were studied in isolated perfused dog hearts, without or with intimal injury induced by means of a balloon catheter inserted into the left anterior descending coronary artery (LAD). Thrombin but not DFP-thrombin induced a dose-dependent PA release in doses of 8 to 32 units. ADP 20 or 200 mumol but not ergonovine 20 or 200 micrograms induced a weak PA release. The local PA activity was much lower in the LAD at 1 or 4 weeks after this injury than in the intact LAD. However, the release of PA from the hearts after intimal injury was similar to findings in the intact hearts. We conclude from this study that thrombin plays an important role in regulating the coagulation-fibrinolysis system in endothelial cells and that changes in the properties of the endothelial cells may lead to initiation and enhancement of atherosclerosis.
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PMID:Release of plasminogen activator from isolated perfused dog heart. 403 71


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