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Results for “Platelet Aggregation”

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At least 19 recordsLinked to original sources

PubMed1975

[Measurement of spontaneous platelet aggregation. Platelet aggregation test III (author's transl)].

A new measuring device for the estimation of the "spontaneous" aggregating activity of thrombocytes has been developed. In this photometric platelet aggregation test (PAT III) a small amount (0.6 ml) of platelet-rich plasma (PRP) is being rotated in a disc-shaped cuvette at 20 rpm, at 37% C. Changes in optical density of PRP which are induced by the formation of platelet aggregates are continuously registered using a chart recorder. The decisive trigger mechanism for aggregation is an increase of plasma pH in the rotating sample which is caused by evaporation of CO2. The results of the test depend on the platelet count in PRP. Aggregation curves are misrepresented by admixture of erythrocytes and lipid turbidity. The tendency of platelets to aggregate increases within 60-90 min following blood sampling. During this period the time interval to the onset of aggregation(Tr) is shortening, and the maximum aggregation speed (alpha2) is increasing. The spontaneously enhanced aggregation tendency of thrombocytes may be reliably measured from 60 min after drawing the blood. The reason for these time-dependent changes which are also demonstrable in ADP-collagen-or epinephrine-induced aggregation is probably the primary shape change of platelets, which occurs after blood drawing and makes them "stickly" and aggregable. PAT III was developed for the detection of enhanced platelet aggregation, indicating a risk of thrombosis and thromboembolic omplications. The new measuring device has been designed as "universal" aggregometer. Additional equipment is available for the registration of ADP-collagen-or epinephrine-induced aggregation similar to Born's and O'Brien's methods. The device may be mounted easily on an Eppendorf photometer without further modifications.

Adenosine Diphosphate↗

PubMed1990

Platelet aggregation, platelet cAMP levels and thromboxane B2 synthesis in patients with diabetes mellitus.

Platelet aggregation, platelet cAMP levels and thromboxane B2 (TXB2) synthesis had been investigated in 40 diabetics (20 with microangiopathy and 20 without) and 24 normal controls. The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. There was no significant difference in platelet aggregation, platelet cAMP levels and platelet TXB2 synthesis between the diabetics with and without microangiopathy. It was suggested that in the diabetic platelets: The observed increase in platelet thromboxane A2 (TXA2) synthesis should be due to the increased activity of arachidonic acid-metabolizing system, most likely at phospholipase site; the elevated platelet TXA2 levels should inhibit platelet membrane-associated adenylate cyclase which lowered the cAMP levels in platelets; and this alternation should be the mechanism of platelet hyperaggregability, which might contribute in some way to diabetic microangiopathy.

Adult↗

PubMed1990

[Effects of tetrandrine on platelet aggregation, platelet adhesion and coagulation].

We examined the effect of tetrandrine on platelet aggregation, platelet adhesion and coagulation in vitro. The results showed that tetrandrine markedly inhibited the platelet aggregation induced by ADP or collagen. Tetrandrine also markedly inhibited platelet adhesion and thrombosis, but didn't change thrombin coagulation time and plasma coagulation time obviously.

Alkaloids↗

PubMed2001

Leukocyte-platelet aggregation, platelet surface P-selectin, and platelet surface glycoprotein IIIa after percutaneous coronary intervention: Effects of dalteparin or unfractionated heparin in combination with abciximab.

BACKGROUND: Plaque disruption with resultant platelet activation and leukocyte-platelet aggregation is a pathophysiologic process common to both acute coronary syndromes and percutaneous coronary interventions. Unfractionated heparin is a standard antithrombotic therapy in patients with both acute coronary syndromes and in those undergoing percutaneous coronary interventions. Low-molecular-weight heparins have been reported to cause less platelet activation than unfractionated heparin. METHODS: Monocyte-platelet aggregates, neutrophil-platelet aggregates, platelet surface P-selectin, and platelet surface glycoprotein (GP) IIIa were measured serially by whole blood flow cytometry in 40 patients with unstable angina (randomly assigned to either unfractionated heparin 70 U/kg or the low-molecular-weight heparin dalteparin 60 IU/kg) undergoing coronary intervention with planned abciximab administration (in 2, one-half-dose boluses). Assays were performed at baseline, 5 minutes after administration of either type of heparin, 10 minutes after the first bolus of abciximab, 10 minutes after second bolus of abciximab, and 8 to 10 and 16 to 24 hours after administration of either heparin. RESULTS: No significant differences in clinical outcomes were observed between patients receiving either unfractionated heparin or dalteparin. The number of circulating P-selectin-positive platelets was increased by unfractionated heparin but not dalteparin, and abciximab reversed this increase. The number of circulating P-selectin-positive platelets was reduced below baseline levels in both treatment groups 8 to 10 and 16 to 24 hours after study drug administration. At 8 to 10 and 16 to 24 hours after administration of study drug, platelet degranulation in response to iso-thrombin receptor agonist peptide 1.5 mmol/L was significantly reduced by almost 50% (compared with immediately after study drug administration). Both unfractionated heparin and dalteparin significantly increased the numbers of circulating monocyte-platelet and neutrophil-platelet aggregates, which were subsequently reduced to baseline levels after administration of the second abciximab bolus and to below baseline at both 8 to 10 and 16 to 24 hours in all patients. After both unfractionated heparin and dalteparin administration, platelet surface GP IIIa expression was significantly increased compared with baseline at both 8 to 10 and 16 to 24 hours. CONCLUSIONS: Dalteparin in combination with abciximab in patients with unstable angina undergoing coronary intervention appears to be safe. Unfractionated heparin, but not dalteparin, degranulates platelets in patients with unstable angina. Both heparins increase the number of circulating monocyte-platelet and neutrophil-platelet aggregates. Abciximab therapy during coronary interventions rapidly reduces the number of degranulated platelets and leukocyte-platelet aggregates.

Abciximab↗

PubMed1983

The effect of aspirin and linoleic acid on platelet aggregation, platelet fatty acid composition and haemostasis in man.

The effect of linoleic acid and of aspirin on platelet aggregation has been measured in six healthy volunteers with a new platelet aggregometer (Wellcome) designed to be used with whole blood. The subjects were given a controlled diet for 6 weeks during which their platelet aggregation, platelet fatty acid composition, dilute blood clot lysis time, bleeding time and serum cholesterol and triglycerides were measured. A basal diet typical of that normally eaten in the UK was fed for 3 weeks, then for a further 2 weeks 60 ml/d of safflower seed oil was added to the diet. Finally there was a further week on the basal diet and on the last day the subjects each took 900 mg of aspirin. The effects of the safflower seed oil was to increase platelet linoleic acid (C18:2 omega 6) content from 5.53 +/- 0.52 micrograms to 10.1 +/- 0.92 micrograms/100 micrograms total fatty acids (P less than 0.001), to decrease platelet aggregation to ADP, and to decreased serum cholesterol. Fibrinolysis and bleeding times were unaltered. Aspirin decreased platelet aggregation, prolonged bleeding time and increased platelet arachidonic acid (C20:4 omega 6) from 24.7 +/- 0.38 micrograms to 25.8 +/- 0.61 micrograms/100 micrograms total fatty acids (P less than 0.01). The Wellcome whole blood aggregometer is a sensitive test of platelet function and using it linoleic acid has been shown to reduce aggregation in conjunction with an increase in polyunsaturated fatty acid content of the platelet membrane.

Adult↗

PubMed1994

The effects of doxazosin on platelet aggregation, platelet adhesion and blood coagulation in cynomolgus monkeys.

The effect of doxazosin, a selective alpha-1 adrenergic inhibitor, on hemostasis was investigated in 9 cynomolgus monkeys. During 12 weeks of doxazosin treatment (1 mg/kg per day), serum lipids, lipoprotein cholesterols, blood coagulation, platelet aggregation and template bleeding times were measured and compared with predrug values. In addition, platelet adhesion to cultured human umbilical vein endothelial cells (HUVEC) in the presence or absence of doxazosin was evaluated. Platelet aggregation was also determined in monkeys following chronic oral exposure to aspirin (162 mg/day). Doxazosin administration was associated with significant reductions in serum total cholesterol (TC) (-16%) and low density lipoprotein cholesterol (LDL-C) (-23%), while high density lipoprotein cholesterol (HDL-C) levels increased 66%. Doxazosin did not alter any parameters of blood coagulation measured; however, bleeding times were increased significantly (33%) in doxazosin-treated animals. Although collagen-stimulated platelet aggregation was not influenced by either chronic doxazosin or aspirin treatment, the maximal extent of ADP-stimulated platelet aggregation was significantly reduced (-26% and -18%, respectively) compared with the control monkeys. Platelets from untreated control animals displayed reductions in the extent of ADP-stimulated aggregation of 13% and 23%, respectively, when incubated in vitro with 200 and 300 micrograms/ml of doxazosin. Additionally, the decrease in aggregation response of platelets obtained from doxazosin-treated monkeys was accompanied by a rapid reversal of platelet aggregation. Adhesion to HUVEC by platelets isolated from doxazosin-treated animals was significantly decreased; however, adhesion was not altered when platelets from untreated control animals were incubated with HUVEC in the presence of doxazosin. Thus, the ex vivo and in vitro studies reported in this communication suggest that doxazosin administration to nonhuman primates is associated with beneficial alterations in plasma lipids, platelet aggregation, bleeding times and platelet adhesion to endothelial cells, parameters which are thought to influence risk of cardiovascular disease in both animals and humans.

Animals↗

PubMed1986

Storage of platelets for tests of platelet function: effects of temperature on platelet aggregation, platelet morphology and liberation of beta-thromboglobulin.

We have studied the effect of temperature on platelets during storage for tests of platelet function. Aliquots of PRP were stored at constant pH at 37 degrees C, room temperature and 4 degrees C. At intervals up to five hours, samples were taken for estimation of platelet shape, plasma levels of beta-thromboglobulin and 14C-serotonin, and assessment of platelet aggregation in response to a range of concentrations of ADP and collagen. When PRP was stored at 37 degrees C there was a gradual decrease in the aggregation response during the period of storage. At room temperature the decrease was slower but the response to ADP often increased dramatically before decreasing; at this temperature there was pronounced liberation of beta TG while there was none at 37 degrees C. Platelets stored at 37 degrees C were smooth and elliptical when examined by electron microscopy, but those stored at room temperature showed partial loss of discoid shape and formation of some pseudopodia. Storage at 4 degrees C was associated with total loss of discoid shape and formation of many large pseudopodia. Light transmission studies also showed loss of discoid shape at room temperature and 4 degrees C. We conclude that storage at 4 degrees C or at room temperature causes platelet activation. To avoid this PRP should be stored at 37 degrees C prior to tests of platelet function.

Blood Platelets↗

PubMed1987

Effects of a 4-week freshwater fish (trout) diet on platelet aggregation, platelet fatty acids, serum lipids, and coagulation factors.

Eight healthy subjects consumed a diet in which all animal products were replaced by 750 g/day of freshwater trout. Platelet eicosapentaenoic acid (EPA) as a percentage of total platelet fatty acids rose from a prediet level of 0.2 +/- 0.4% to 3.4 +/- 1.6% after 4 weeks on the diet. Platelet arachidonic acid remained unchanged. Platelets became more hyperaggregable to collagen (p less than .025) but became hypoaggregable to arachidonic acid (p less than .05). The Ivy bleeding time became prolonged rising from a mean of 148 seconds before the diet to 168 seconds at 2 weeks and 202 seconds at 4 weeks. Serum lipids, coagulation profiles, and blood pressure remained unchanged. The changes induced by this diet were much less marked than changes induced by marine fish diets and diets supplemented by marine fish oil extracts, despite the fact that an equivalent amount of EPA was consumed and incorporated into platelets. These findings suggest that other substances, in addition to n-3 unsaturated fatty acids, may be responsible for the antithrombotic properties of marine fish.

Adult↗

PubMed1982