Modulation of Platelet Function by Prostaglandins: Characterization of Platelet Receptors for Stimulatory Prostaglandins and the Role of Arachidonate Metabolites in Platelet Degranulation Responses

MacIntyre, D. Euan

doi:10.1159/000214318

Cited by 11 publications

(2 citation statements)

References 22 publications

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“…MacIntyre [18] has postulated the exis tence o f a thromboxane receptor, and a fail ure o f the patients' platelets to aggregate in response to U44069 and the other agents which act by the thromboxane pathway sug gests an abnormality o f interaction with the thromboxane receptor. It is possible that the increased production o f thromboxane by platelets from myeloproliferative patients re flects an attempt to overcome this defect.…”

Section: Discussionmentioning

confidence: 99%

Platelet Thromboxane Synthesis and Release Reactions in Myeloproliferative Disorders

Smith¹,

Martın²

1982

Pathophysiol Haemos Thromb

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A group of patients with myeloproliferative disorders was studied with respect to platelet aggregation responses, release of β-thromboglobulin and incorporated 5-hydroxy-tryptamine, and synthesis of thromboxane B₂. In all patients the resting plasma β-thrombo-globulin was elevated. Aggregation responses were frequently impaired to adrenaline, arachi-donic acid, A23187 and the prostaglandin endoperoxide analogue, U44069. Both 5-hydroxy-tryptamine and β-thromboglobulin release were greater with patients’ platelets than with those of controls in response to adrenaline, ADP and U44069. The patients’ platelets produced more thromboxane B₂ than did controls, irrespective of the agonist used, yet those aggregating agents which are thought to act by generating thromboxane A₂ were relatively ineffective in causing aggregation. This might reflect resistance to thromboxane A₂ action in these patients, which is met by increased thromboxane formation.

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Section: Discussionmentioning

confidence: 99%

Platelet Thromboxane Synthesis and Release Reactions in Myeloproliferative Disorders

Smith¹,

Martın²

1982

Pathophysiol Haemos Thromb

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“…All these harmful side effects of hemodialysis can be prevented by prostacyclin, a naturally occurring metabo lite of arachidonic acid produced by vascular endothelia [19][20][21], It enhances the level of platelet cyclic adenosine monophosphate and thereby inhibits platelet aggrega tion and release of the platelet coagulation factors [21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Effect of Heparin and Prostacyclin/Heparin Infusion on Platelet Aggregation in Hemodialyzed Patients

Kuźniewski¹,

Sułowicz²,

Hanicki³

et al. 1990

Nephron

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The number of circulating platelet aggregates determined according to the method of Wu and Hoak and the platelet morphology revealed by scanning electron microscopy were investigated in 10 patients (8 males, 2 females) age 28–58 years) with end-stage renal failure treated by repeated hemodialysis. The examination was carried out twice: during a 4-hour hemodialysis session with the use of heparin alone and 1 week later during the course of another dialysis in the presence of both heparin and prostacyclin. During each dialysis session the platelet system was examined three times: prior to, after 90 min, and at the end of the procedure. As compared with the situation prior to dialysis, the number of platelet aggregates assessed after 90 min of dialysis and after its termination insignificantly rose following the treatment with heparin, but significantly fell after the use of the prostacyclin/heparin combination. The differences were also significant when the effects of both treatment types were compared. As revealed by scanning electron microscopy, during the course of hemodialysis with the use of heparin alone, the platelets showed signs of activation manifested by increases in number and length of cytoplasmic processes and by a tendency to aggregate. When both prostacyclin and heparin were used during dialysis, platelet activation was minimal or absent. Thus, the combined treatment with prostacyclin and heparin protects platelets from activation induced by their contact with artificial surfaces and may lower the risk of microthrombosis, making thereby hemodialysis safer and more effective.

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Stereo-dependent inhibition of human platelet function by the optical isomers of trimetoquinol

Mayo

Navran

Huzoor-Akbar

et al. 1981

Biochemical Pharmacology

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Modulation of Platelet Function by Prostaglandins: Characterization of Platelet Receptors for Stimulatory Prostaglandins and the Role of Arachidonate Metabolites in Platelet Degranulation Responses

Cited by 11 publications

References 22 publications

Platelet Thromboxane Synthesis and Release Reactions in Myeloproliferative Disorders

Platelet Thromboxane Synthesis and Release Reactions in Myeloproliferative Disorders

Effect of Heparin and Prostacyclin/Heparin Infusion on Platelet Aggregation in Hemodialyzed Patients

Stereo-dependent inhibition of human platelet function by the optical isomers of trimetoquinol

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