Bleeding Time after Aspirin in Disorders of Intrinsic Clotting

Kaneshiro, Marc; Mielke, C. Harold; Kasper, Carol K.; Rapaport, Samuel I.

doi:10.1056/nejm196911062811904

Cited by 120 publications

(28 citation statements)

References 10 publications

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“…Even using collagen, where aspirin treatment does inhibit the release reaction, higher concentrations' of collagen overcome aspirin inhibition (23). However, prostaglandins are important in vivo since aspirin induces a mild hemostatic defect in normal individuals, and in patients with defects in intrinsic coagulation, a much more severe defect is produced (25). If not essential for aggregation and release, prostaglandins may serve as modifiers of platelet function, the effects of which could be important in pathological states such as myocardial infarction (26).…”

Section: Discussionmentioning

confidence: 99%

Cyclic adenosine 3',5'-monophosphate inhibits the availability of arachidonate to prostaglandin synthetase in human platelet suspensions.

Minkes¹,

Stanford²,

M³

et al. 1977

J. Clin. Invest.

276

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A B S T R A C T When thrombin is added to washed human platelets, one of its actions results in activation of a phospholipase that hydrolyzes arachidonic acid from phospholipids. The arachidonate is converted to the cyclic endoperoxides (prostaglandin G2 and prostaglandin H2) by fatty acid cyclo-oxygenase. These compounds are then converted to thromboxane A2, also called rabbit aorta-contracting substance, by thromboxane synthetase. These labile, pharmacologically active compounds then break down to inactive products including thromboxane B2 and malonaldehyde. Incubation of platelets with either dibutyryl cyclic adenosine 3',5'-monophosphate (dBcAMP) or prostaglandin E, (PGE,) before thrombin addition blocks the subsequent formation of oxygenated products of arachidonic acid including thromboxane A2, thromboxane B2, and malonaldehyde. In contrast, when arachidonic acid is added directly to platelets, prior incubation with dBcAMP or PGE, does not inhibit production of the prostaglandins or their metabolites. Thrombin treatment of platelets also blocks the acetylation of cyclo-oxygenase by aspirin since the hydrolyzed arachidonic acid competes with aspirin for the active site on cyclo-oxygenase. Prior treatment of platelets with dBcAMP or PGE, reverses the thrombin inhibition of the acetylation of cyclo-oxygenase. We conclude that agents which elevate platelet cAMP levels inhibit the hydrolysis of arachidonic acid from platelet phospholipids. We also find that prostaglandin synthesis can be dissociated, in part, from platelet aggregation and release, and that cAMP has separate actions on these processes. Higher thrombin concentrations are required to stimu-

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Section: Discussionmentioning

confidence: 99%

Cyclic adenosine 3',5'-monophosphate inhibits the availability of arachidonate to prostaglandin synthetase in human platelet suspensions.

Minkes¹,

Stanford²,

M³

et al. 1977

J. Clin. Invest.

276

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“…The effect of aspirin on platelets has been studied at many levels. Clinically, aspirin has modest effects on hemostasis in normal individuals (1) but may induce markedly prolonged bleeding times in hemophiliacs (2). When platelet function is studied in vitro, aspirin has been shown to inhibit the platelet release reaction.…”

Section: Introductionmentioning

confidence: 99%

The mechanism of the effect of aspirin on human platelets. I. Acetylation of a particulate fraction protein.

Roth¹,

Majerus²

1975

J. Clin. Invest.

816

268

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A B S T R A C T Aspirin (acetylsalicylic acid) inhibits platelet prostaglandin synthesis and the ADP-and collagen-induced platelet release reaction. [acetyl-'H]aspirin radioactivity paralleled that of platelet turnover. Therefore, in addition to its saturability, acetylation of the particulate fraction protein by aspirin was permanent.In two respects, the inhibition of platelet function by aspirin correlates well with the aspirin-mediated acetylation of the particulate fraction protein. Both per-

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“…The mechanism for spontane ous hemothorax in hemophilia is unknown although spontaneous hemothorax has been reported in pa tients with hemophilia [1][2][3][4][5][6] and as a complication of anticoagulation therapy [7]. Aspirin prolongs the bleeding time in patients with hemophilia and serious bleeding can result [8]. Aspirin interferes with platelet function and may have increased the bleeding tend ency in the 1st patient.…”

Section: Discussionmentioning

confidence: 99%

Hemothorax and Hemomediastinum in Patients with Hemophilia

et al. 1985

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Three patients with hemophilia presented with hemothoraces which resolved within 1–3 weeks following treatment with factor concentrates. Drainage of blood was not necessary. Eight previously reported cases are reviewed, and therapy and complications are summarized. We suggest that treatment of this rare complication of hemophilia with factor concentrates and avoidance of surgical intervention is indicated.

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Bleeding Time after Aspirin in Disorders of Intrinsic Clotting

Cited by 120 publications

References 10 publications

Cyclic adenosine 3',5'-monophosphate inhibits the availability of arachidonate to prostaglandin synthetase in human platelet suspensions.

Cyclic adenosine 3',5'-monophosphate inhibits the availability of arachidonate to prostaglandin synthetase in human platelet suspensions.

The mechanism of the effect of aspirin on human platelets. I. Acetylation of a particulate fraction protein.

Hemothorax and Hemomediastinum in Patients with Hemophilia

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