Effects of Salicylates on Human Platelets

O'Brien, J.R.

doi:10.1016/s0140-6736(68)92228-9

Cited by 526 publications

(150 citation statements)

References 11 publications

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“…This antagonism to the effects of TxA2 should explain the interference of alkaline phosphatase with the second wave of ADP-induced aggregation, which is suppressed by thromboxane agonists and cyclo-oxygenase inhibitors (O'Brien, 1968;Mills et al, 1974;Armstrong et al, 1985). Those inhibitors are also effective against the second wave of adrenaline-induced aggregation (O'Brien, 1968;Armstrong et al, 1985), which was surprisingly not modified by alkaline phosphatase. This unexpected dissociation between ADP and adrenaline is probably accounted for by different locations of their receptor site(s) within the membrane and/or by divergent transduction mechanisms underlying platelet activation even though in both cases cyclo-oxygenase-dependent metabolites of arachidonate are involved.…”

Section: Discussionmentioning

confidence: 96%

Alkaline phosphatase prevents platelet stimulation by thromboxane‐mimetics

Hatmi

Haye

Gavaret

et al. 1991

British J Pharmacology

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1 The effects of alkaline phosphatase on platelet aggregation, secretion and thromboxane B2 (TxB2) generation induced by the full dose-range of common platelet agonists were studied in human platelet-rich plasma and washed platelets. 2 Platelet aggregation and adenosine 5'-triphosphate (ATP) secretion induced by threshold and supramaximal concentrations of arachidonate and stable TxA2 and prostaglandin endoperoxide-mimetics (compounds U46619 and EP171) were abolished in the presence of alkaline phosphatase (0.5-1 u ml 1), even though the synthesis of TxB2 persisted. In contrast, platelet aggregation by PAF-acether and by supramaximal concentrations of thrombin as well as the primary wave of aggregation by adenosine diphosphate (ADP) and adrenaline were unaffected by alkaline phosphatase under conditions where the secondary wave of aggregation by ADP was blocked. 3 Alkaline phosphatase, unlike prostacyclin, failed to raise the adenosine 3': 5'-cyclic monophosphate (cyclic AMP) content of the platelets. Also, the pretreatment of platelets by inorganic phosphate or by ATP plus creatine phosphate/creatine phosphokinase reversed the inhibitory effect of alkaline phosphatase.4 Experiments performed in the guinea-pig in vivo showed that alkaline phosphatase was effective on thrombocytopenia induced by arachidonate. 5 Our results provide the first direct evidence for a specific inhibitory effect of alkaline phosphatase at a site sensitive to TxA2 and prostaglandin endoperoxides and suggest that its phosphorylation/ dephosphorylation state may play an important role in modulating platelet activation. These results also suggest the presence of ecto-protein kinases on membrane platelets.

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Section: Discussionmentioning

confidence: 96%

Alkaline phosphatase prevents platelet stimulation by thromboxane‐mimetics

Hatmi

Haye

Gavaret

et al. 1991

British J Pharmacology

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“…While the inhibitory effect of acetylsalicylic acid on platelet function (O'Brien, 1968;Weiss et al, 1968;Zucker & Peterson, 1970) and prostanoid formation (Smith & Willis, 1971;Vane, 1971) is well known (Atkinson & Collier, 1980), the effects of sodium salicylate are much less defined. Although salicylate has been shown to be similarly potent as an analgesic and anti-inflammatory drug (Atkinson & Collier, 1980; Rainsford, 1984), it has almost no effect on prostanoid formation of gastric mucosa (Ligumsky et al, 1982;Whittle et al, 1980), macrophages (Kuehl et al, 1980), ram seminal vesicle microsomes (Humes et al, 1981), or thrombocytes (Roberts et al, 1984;Smith & Willis, 1971;Vargaftig, 1978a).…”

Section: Introductionmentioning

confidence: 99%

Effects of salicylic and acetylsalicylic acid alone and in combination on platelet aggregation and prostanoid synthesis in man.

Rosenkranz¹,

Fischer²,

Meese³

et al. 1986

Brit J Clinical Pharma

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The present study was designed to investigate the effects of salicylate on the antiplatelet action of acetylsalicylic acid as well as on in vivo prostanoid formation and platelet function in healthy volunteers. In the first study six female volunteers received 350 mg acetylsalicylic acid intravenously, with and without previous oral administration of sodium salicylate (1200 mg daily for 3 days). Urinary prostanoid excretion as well as platelet aggregation and thromboxane formation were measured before and during salicylate and after acetylsalicylic acid. In the second study seven female volunteers received sodium salicylate (52.6 mg kg‐1) or acetylsalicylic acid (60.7 mg kg‐1) for 8 days in a randomized cross‐over protocol. Urinary prostanoid excretion, platelet aggregation and thromboxane formation as well as salicylate plasma concentrations were determined before, during and after administration of each drug. Sodium salicylate did not impair the complete suppression of arachidonic acid‐induced platelet thromboxane formation and aggregation obtained by the single intravenous dose of acetylsalicylic acid in the first study. Sodium salicylate in the second study did not affect urinary excretion of prostaglandin E2, its major urinary metabolite (7 alpha‐hydroxy‐5,11‐ diketo‐tetranor‐prostane‐1,16‐dioic acid), and 2,3‐dinor‐6‐keto‐ prostaglandin F1 alpha, the main urinary metabolite of epoprostenol (prostacyclin, PGI2). In contrast, acetylsalicylic acid significantly decreased excretion rates of these prostanoids by 64, 59 and 61%, respectively. In both studies platelet aggregation and thromboxane formation induced by collagen, thrombin or arachidonic acid were not significantly affected by salicylate administration, whereas acetylsalicylic acid inhibited platelet aggregation induced by all three agents as well as thrombin‐ and arachidonic acid induced thromboxane formation.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…9) Pseudoaneurysm often occurs in the arteries with a superficial course, with rather small calibers, and/or injury with a small needle. Stopping of aspirin administration, 1,13,15) change from unfractionated heparin to nafamostat mesilate, 12) and/or thrombogenicity of nonionic iodinated contrast medium 3) might promote aneurysmal thrombosis, but spontaneous resolution of unknown etiology is most likely. A period of Neurol Med Chir (Tokyo) 49, November, 2009…”

Section: Discussionmentioning

confidence: 99%

Spontaneous Resolution of Delayed Onset Large Subclavian Artery Pseudoaneurysm -Case Report-

Ohta

Maekawa

Kasuno

et al. 2009

Neurol. Med. Chir.(Tokyo)

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A 70-year-old woman with a history of end-stage renal disease secondary to anti-neutrophil cytoplasmic autoantibody-associated vasculitis had been receiving hemodialysis for 5 years. The patient underwent attempted right internal jugular vein cannulation for temporary hemodialysis catheter placement. Pulsating mass developed in the neck and angiography revealed a subclavian artery pseudoaneurysm 4 days later. The pseudoaneurysm disappeared spontaneously during the interval between the diagnosis and the planned surgical procedure. Such delayed onset and spontaneous resolution of subclavian artery pseudoaneurysm is uncommon. Close observation may be optimal if delayed onset of pseudoaneurysm occurs after small needle puncture with cessation of antiplatelet/anticoagulant administration.

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Effects of Salicylates on Human Platelets

Cited by 526 publications

References 11 publications

Alkaline phosphatase prevents platelet stimulation by thromboxane‐mimetics

Alkaline phosphatase prevents platelet stimulation by thromboxane‐mimetics

Effects of salicylic and acetylsalicylic acid alone and in combination on platelet aggregation and prostanoid synthesis in man.

Spontaneous Resolution of Delayed Onset Large Subclavian Artery Pseudoaneurysm -Case Report-

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