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Alteration of the response of platelets to surface stimuli by pyrazole compounds.

TLDR
It was found that phenylbutazone prolonged platelet survival to more than twice the normal time and reduced platelet turnover by nearly 50%.
Abstract
Sulfinpyrazone and phenylbutazone block the aggregating action of collagen, antigen-antibody complexes, and gamma globulin-coated surfaces on blood platelets. These drugs do not block the action of ADP or thrombin. Inhibition of surface-induced aggregation appears to be the result of a decreased response of the platelets to surface stimuli, giving rise to diminished release of platelet constituents, such as ADP and serotonin. The intravenous infusion of these drugs produced results similar to those found in the in vitro experiments. Administration of phenylbutazone in doses sufficient to produce marked suppression of the platelet-collagen reaction impaired hemostatic plug formation at the ends of transected mesenteric vessels in rabbits. Since platelet function is considered a factor influencing platelet survival, the effect of phenylbutazone on platelet survival was examined. It was found that phenylbutazone prolonged platelet survival to more than twice the normal time and reduced platelet turnover by nearly 50%. These studies show that drugs which suppress platelet response to surface stimuli alter platelet function in vivo.

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Controlled trial of aspirin in cerebral ischemia.

TL;DR: It cannot be inferred from this study that aspirin prevents stroke because when end points were restricted to death or cerebral or retinal infarction, there was no statistically significant differential between the aspirin and placebo treatments.
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The effect of salicylates on the hemostatic properties of platelets in man

TL;DR: These studies lend further support to the hypothesis that ingestion of aspirin, in contrast to sodium salicylate, prolongs the bleeding time by inhibiting the release of platelet ADP, perhaps reflecting the findings in other cell systems which suggest that aspirin alters membrane permeability.
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Adenosine diphosphate-induced platelet aggregation in suspensions of washed rabbit platelets.

TL;DR: On comparison with rabbit platelets prepared from blood taken into EDTA, the only differences observed were the much greater sensitivity to ADP and a higher calcium content; platelet morphology, nucleotide levels, and conversions of 14C‐ATP and 14C-ADP at the platelet membrane were similar.
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Factors responsible for ADP-induced release reaction of human platelets

TL;DR: Although fibrinogen is required for ADP-induced primary aggregation, it does not support secondary aggregation and release, provided that it has no clot-promoting activity.
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The effect of plasma proteins on the interaction of platelets with glass surfaces.

TL;DR: In this paper, the presence of gelatin in the medium in which washed platelets are suspended decreases the adherence of platelets to surfaces, although it does not diminish the extent of release of platelet contents induced by gamma globulin-coated tubes.
References
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Journal Article

The physiological disposition of phenylbutazone (butazolidin) in man and a method for its estimation in biological material

TL;DR: After discontinuance of dosage, the rate of biotransformation in man is slow, averaging about 20 per cent per day, but varies considerably in different subjects, and different species vary markedly in the rates at which they metabolize phenylbutazone.
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Platelet Clumping Produced by Connective Tissue Suspensions and by Collagen.

TL;DR: Saline suspensions of a variety of connective tissues and of collagen clump platelets in citrated platelet-rich plasma even in dilutions of 1:100, and the probable role of the connective tissue factor in hemostasis is discussed.
Journal ArticleDOI

Mechanism of platelet plug formation and role of adenosine diphosphate.

TL;DR: Traumatized rat omentum was used to demonstrate the development of "platelet plugs" following agitation in platelet-rich plasma, and in the absence of divalent cation there was only platelet adhesion to plasma.