The role of arachidonate lipoxygenase and fatty acids during irreversible blood platelet aggregation in vitro

Dutilh, C.E.; Haddeman, E; Don, J.A.; Hoor, F. ten

doi:10.1016/0161-4630(81)90081-1

Cited by 67 publications

(13 citation statements)

References 22 publications

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“…Piroxicam produced less inhibition than indomethacin ( Figure 5). Indomethacin also inhibits platelet lipoxygenase (Siegel, McConnell & Cuatrecasas, 1979) the products of which may have a role in irreversible platelet aggregation (Dutilh, Haddeman, Don & Ten Hoor, 1981). In addition, indomethacin has a calcium antagonistic action (Northover, 1977).…”

Section: Discussionmentioning

confidence: 99%

In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti‐inflammatory drugs

Mallarkey

Smith

1984

British J Pharmacology

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Using the Technicon Autocounter, the mechanisms involved in collagen‐induced platelet aggregation in vivo have been studied without the interference of an anticoagulant. Extracellular divalent cation was essential for in vivo platelet aggregation. Non‐steroidal anti‐inflammatory drugs completely inhibited the aggregation induced by collagen in platelet‐rich plasma in in vitro or ex vivo studies. In vivo only a maximum of 50% inhibition was achieved when release of thromboxane A2 (TXA2) was completely inhibited. Therefore in vivo, collagen causes aggregation through more than one pathway which operate independently of each other and which are all dependent on extracellular divalent cation. In vivo, when different doses of collagen were compared, aggregation produced by low doses of collagen was more dependent upon prostaglandin endoperoxide/TXA2 formation.

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Section: Discussionmentioning

confidence: 99%

In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti‐inflammatory drugs

Mallarkey

Smith

1984

British J Pharmacology

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“…Literature data on platelet aggregation arc dis cordant but most studies are in favor of an increased aggregability [3.4] possibly due to abnormalities in arachidonic acid metabolism [5,6], To our knowledge, no previous report on platelet adhesivity is available. We demonstrate here a strong defect of this function in psoriasis.…”

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confidence: 99%

Primary Hemostasis, Platelet Functions and Coagulation in Psoriasis

Dandurand

Rouanet²,

Morcrete

et al. 1989

Dermatology

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“…Moreover, this 5-HT-mediated platelet activation is not affected by the cyclo-oxygenase inhibitors suprofen and indomethacin, the thromboxane A2 synthetase inhibitors R 19 091 and dazoxiben, the combined cycto-oxygenase/lipoxygenase inhibitors BW755C and N.D.G.A. Such findings makes a contribution of prostaglandin endoperoxides or thromboxane A2 as intercellular or intracellular mediators [12,22] or lipoxygenase products [23] for platelet reactions to 5-HT unlikely.…”

Section: Compoundmentioning

confidence: 94%

Biochemical mechanisms in 5-hydroxytryptamine-induced human platelet aggregation

Xhonneux

1985

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The activation of human platelets by 5-hydroxytryptamine (5-HT) is not accompanied by detectable release of ATP or TXB2. The process is unaffected by cyclooxygenase, thromboxane synthetase or combined cyclooxygenase/lipoxygenase inhibition (suprofen, indomethacin, R 19091, dazoxiben, N.D.G.A, BW755C, esculetin), indicating the absence of involvement of arachidonic acid metabolites. Transmembrane Ca2+-entry blockers (flunarizine, nifedipine, nimodipine) have no effect either, indicating that the activator calcium released by 5-HT comes from intracellular stores. The 5-HT-induced platelet activation is inhibited by stimulators of adenylate cyclase (PGE1, PGE2, isoprenaline, adenosine) and inhibitors of cAMP phosphodiesterase (papaverine, anagrelide, RA233), indicating that also for this type of platelet activation cAMP behaves as a unidirectional, inhibitory regulator.

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The role of arachidonate lipoxygenase and fatty acids during irreversible blood platelet aggregation in vitro

Cited by 67 publications

References 22 publications

In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti‐inflammatory drugs

In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti‐inflammatory drugs

Primary Hemostasis, Platelet Functions and Coagulation in Psoriasis

Biochemical mechanisms in 5-hydroxytryptamine-induced human platelet aggregation

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