Thrombus induction by endogenic PAF-acether and its inhibition by Ginkgo Biloba extracts in the guinea pig

Bourgain, R.H.; Maes, L.; Andries, R.; Braquet, P.

doi:10.1016/0090-6980(86)90157-7

Cited by 16 publications

(5 citation statements)

References 6 publications

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“…Several studies by Pierre Braquet and colleagues demonstrated that one compound in particular, BN 2021, was a highly specific competitive PAF antagonist. Several related ginkgolides also exhibited inhibitory properties against PAF [195,196,197,198,199,200]. Indeed, several other researchers at the time discovered anti-PAF properties in other natural isolates of Chinese medicinal herbs such as phomactin A, kadsurenone, and various xanthones [201,202,203,204,205].…”

Section: The Potential Use Of Platelet-activating Factor Inhibitormentioning

confidence: 99%

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

2019

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In the late 1960s, Barbaro and Zvaifler described a substance that caused antigen induced histamine release from rabbit platelets producing antibodies in passive cutaneous anaphylaxis. Henson described a ‘soluble factor’ released from leukocytes that induced vasoactive amine release in platelets. Later observations by Siraganuan and Osler observed the existence of a diluted substance that had the capacity to cause platelet activation. In 1972, the term platelet-activating factor (PAF) was coined by Benveniste, Henson, and Cochrane. The structure of PAF was later elucidated by Demopoulos, Pinckard, and Hanahan in 1979. These studies introduced the research world to PAF, which is now recognised as a potent phospholipid mediator. Since its introduction to the literature, research on PAF has grown due to interest in its vital cell signalling functions and more sinisterly its role as a pro-inflammatory molecule in several chronic diseases including cardiovascular disease and cancer. As it is forty years since the structural elucidation of PAF, the aim of this review is to provide a historical account of the discovery of PAF and to provide a general overview of current and future perspectives on PAF research in physiology and pathophysiology.

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Section: The Potential Use Of Platelet-activating Factor Inhibitormentioning

confidence: 99%

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

2019

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“…In the underlying arterial thrombotic process, PAF plays a critical role in the pathogenesis of thrombosis as it is an activator of committed cells, leukocytes, platelets, and endothelial cells (HIRAFUJI and SHINODA 1991). By superfusion of the mesenteric artery with PAF, thrombosis can be induced (BOURGAIN et al 1985(BOURGAIN et al , 1986, and P AF antagonists have protective effects on pulmonary microembolism (KLEE et al 1991) and on other types of thrombosis models, especially in mice and cats (SETH et al 1994). The same PAF antagonists had no effect in a model of venous thrombosis (SETH et al 1994).…”

Section: Thrombovascular Diseasesmentioning

confidence: 99%

Pathological Aspects of Platelet-Activating Factor (PAF)

Bruchhausen¹

1997

Platelets and Their Factors

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“…A damaging effect on the platelet membrane is unlikely since the response to PAF was dose dependent. PAF is a potent inducer of platelet activation, 25 -thrombosis, 28 and ischemia 29 and has been postulated to play an important role in the pathogenesis of microangiopathy. 30 - 31 Therefore, suppression of PAFinduced platelet responses, in addition to those of thrombin and collagen induction, may be necessary to more effectively limit pathologic thrombosis.…”

Section: Activated Cytoplasmic Ionized Calcium Concentrationmentioning

confidence: 99%

Baseline and activated platelet cytoplasmic ionized calcium in acute ischemic stroke. Effect of aspirin.

Joseph

Welch

Grunfeld

et al. 1988

Stroke

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O ne reason for the limited usefulness of aspirin in the treatment of ischemic stroke may be that aspirin does not suppress platelet responsiveness to all in vivo thrombogenic stimuli. Among the known in vivo mediators of platelet activation, thrombin, collagen, and platelet activating factor (PAF) are believed to be important. Cytoplasmic ionized calcium is the pivotal second messenger coupling platelet stimulation and response.1 Therefore, we studied the effect of aspirin treatment on cytoplasmic ionized calcium concentration ( [Ca,2+ ]) following stimulation with thrombin, collagen, and PAF. Baseline and stimulated [Caj 2+ ] is reliably measured by loading washed platelets with aequorin, a Ca 2+ -sensitive photoprotein.2 -4 Using this technique, we show that the increase in [Ca,2+ ] following stimulation with PAF is not suppressed by aspirin treatment. Subjects and MethodsWe studied 25 healthy people (nine men, 16 women) ranging in age from 20 to 74 (mean±SD 45 ±14) From years. These controls were free of all antiplatelet medication (aspirin, nonsteroidal anti-inflammatory drugs) for at least 10 days before the study. We also studied 26 patients with acute ischemic stroke (13 men, 13 women) ranging in age from 24 to 88 (mean±SD 55 ±17) years. The patients were also free of all antiplatelet medications for at least 10 days before the study (untreated). Twelve patients had large, cortical infarcts attributed to majorvessel occlusion and 14 had small, subcortical infarcts attributed to small-vessel occlusion; the diagnosis was based on clinical examination and was supported by computed tomography, magnetic resonance imaging, or four-vessel cerebral angiography. Nine patients were studied ^24 hours, nine 36-72 hours, and eight 4-35 days after the onset of neurologic dysfunction. Sixteen patients suffered from essential hypertension, one had insulindependent diabetes mellitus and hypertension, and nine had neither; treatment of hypertension was limited to thiazide diuretics and/or clonidine.In addition, we studied 12 patients with acute ischemic stroke (nine men, three women) treated with 325 mg/day aspirin for 1-4 days. These aspirintreated patients ranged in age from 39 to 82 (mean±SD 64 ±15) years and were studied within 96 hours after the onset of neurologic dysfunction.Sixty milliliters of blood from the antecubital vein was collected from all subjects in the resting state by guest on May 9, 2018 http://stroke.ahajournals.org/ Downloaded from

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Thrombus induction by endogenic PAF-acether and its inhibition by Ginkgo Biloba extracts in the guinea pig

Cited by 16 publications

References 6 publications

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

Forty Years Since the Structural Elucidation of Platelet-Activating Factor (PAF): Historical, Current, and Future Research Perspectives

Pathological Aspects of Platelet-Activating Factor (PAF)

Baseline and activated platelet cytoplasmic ionized calcium in acute ischemic stroke. Effect of aspirin.

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