C0417: Bleeding Propensity by Ticagrelor and Clopidogrel at Similar Inhibition of Platelet Aggregation in a Conscious Pig Model

Summary“Early” fibrinogen degradation products are more potent inhibitors of thrombin-induced clotting than “late” products and also interfere with the ability of thrombin to release serotonin from platelets. “Early” and “intermediate” FDP cause moderate inhibition of platelet aggregation induced by adenosine diphosphate or connective tissue particles. Serotonin release by connective tissue particles is probably not inhibited by FDP.

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Effects of Halothane on Platelet Function

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650105 ◽

1980 ◽

Vol 44 (03) ◽

pp. 143-145 ◽

Cited By ~ 19

Author(s):

J Dalsgaard-Nielsen ◽

J Gormsen

Keyword(s):

Platelet Aggregation ◽

Platelet Function ◽

Platelet Rich Plasma ◽

Human Platelets ◽

Halothane Anaesthesia ◽

Inhibition Of Platelet Aggregation ◽

Transient Impairment ◽

High Concentrations ◽

Uptake And Release ◽

Platelet Functions

SummaryHuman platelets in platelet rich plasma (PRP) incubated at 37° C with 0.3–2% halothane for 5–10 min lost the ability to aggregate with ADP, epinephrine and collagen.At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible.The results suggest that halothane anaesthesia produces a transient impairment of platelet function.

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Inhibition of Fibrinolytic Activity In-Vivo by Dexamethasone Is Counterbalanced by an Inhibition of Platelet Aggregation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656320 ◽

1992 ◽

Vol 68 (01) ◽

pp. 069-073 ◽

Cited By ~ 16

Author(s):

J J J van Giezen ◽

J W C M Jansen

Keyword(s):

Platelet Aggregation ◽

Fibrinolytic Activity ◽

Ex Vivo ◽

Dose Range ◽

Coagulation System ◽

Loop Model ◽

Prothrombotic State ◽

Inhibition Of Platelet Aggregation ◽

Pai 1

SummaryDexamethasone decreases the fibrinolytic activity in cultured medium of several cell types by an induction of PAI-1 synthesis. As a result of this enhanced PAI-1 synthesis a prothrombotic state is expected in patients treated with dexamethasone. However, such a prothrombotic state is not reported as a major adverse effect. We have studied the effects of dexamethasone (dose range: 0.1–3.0 mg/kg) on the fibrinolytic system of rats after a 5 day pretreatment period. It appeared that dexamethasone dose dependently decreased the fibrinolytic activity (a dose of 1 mg/kg showed a reduction of about 40%). This reduced fibrinolytic activity could be functionally translated into an increased thrombus size as measured with a venous thrombosis model: thrombus size was increased by 50% with 1 mg/kg dexamethasone. No effects could be measured on the coagulation system, but it appeared that ex-vivo measured platelet aggregation was dose dependently inhibited by dexamethasone treatment. This effect resulted in-vivo in prolonged obstruction times as measured with a modified aorta-loop model. These results indicate that the expected prothrombotic state due to a diminished fibrinolytic activity caused by dexamethasone is counterbalanced by an inhibition of platelet aggregation.

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Inhibition of Platelet Aggregation by Human Placenta

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657866 ◽

1985 ◽

Vol 54 (02) ◽

pp. 431-437 ◽

Cited By ~ 1

Author(s):

M J Dembélé-Duchesne ◽

A Laghchim Lahlou ◽

H Thaler-Dao ◽

A Crastes de Paulet

Keyword(s):

Fatty Acid ◽

Platelet Aggregation ◽

Human Placenta ◽

Cyclooxygenase Inhibitor ◽

Synthetase Inhibitor ◽

Inhibition Of Platelet Aggregation ◽

Thromboxane Synthetase ◽

Rabbit Platelets ◽

High Doses ◽

Induced Aggregation

SummaryHuman placental cytosol inhibits platelet aggregation induced by high doses of collagen. The aim of this study was to investigate whether this anti-aggregating activity was caused only by the presence of various activities already described in the placenta (an ADP-consuming enzyme, a fatty acid cyclooxygenase inhibitor, and a thromboxane synthetase inhibitor) or whether another factor was present.Heating the cytosol at 50° C for 6 min destroyed the inhibitor of collagen-induced aggregation. ADPase and the AA pathway inhibitors were not modified by this treatment. We therefore show the presence of an additional anti-aggregating factor: it is destroyed by heating at 50° C.We also tested for the presence of an inhibitor of AA release in the placental cytosol using three different methods (rabbit platelets in PRP, washed rabbit platelets, and NRK fibroblasts) but no inhibition could be evidenced.We conclude that this new anti-aggregating factor, which is probably a protein, acts neither through AA release inhibition nor AA cascade inhibition.

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The Increased Sensitivity of Platelets to Prostacyclin in Marathon Runners

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661107 ◽

1984 ◽

Vol 51 (03) ◽

pp. 385-387 ◽

Cited By ~ 8

Author(s):

Clive J Dix ◽

David G Hassall ◽

K Richard Bruckdorfer

Keyword(s):

Cardiovascular Disease ◽

Endothelial Cells ◽

Platelet Aggregation ◽

Cyclic Amp ◽

Adenylate Cyclase ◽

Platelet Rich Plasma ◽

Marathon Runners ◽

Inhibition Of Platelet Aggregation ◽

Increased Sensitivity ◽

Membrane Bound

SummaryPlatelet-rich plasma was obtained 24 hr after the race ended from athletes who ran in the London marathon. The platelets were only marginally less sensitive to adrenaline than were those of non-runners using conventional aggregation tests. However, the runners’ platelets were much more sensitive to inhibition by prostacyclin, a prostaglandin synthesized by endothelial cells. It appeared that this effect was due to a greater activity in the platelets of the membrane-bound adenylate cyclase enzyme which generates intracellular cyclic AMP. Cyclic AMP production is known to be stimulated by prostacyclin and to cause the inhibition of platelet aggregation. The results indicate another possible protective effect of exercise against cardiovascular disease which is independent of the known changes in lipoprotein concentrations previously observed in athletes.

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