Studies on the stimulation of human blood platelets by semisynthetic platelet-activating factor

Ostermann, G; Till, U; Thielmann, K

doi:10.1016/0049-3848(83)90235-9

Cited by 30 publications

(3 citation statements)

References 13 publications

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“…Platelet-activating factor (Paf-acether, 1-alkyl-2acetyl-sn-glycero-3-phosphorylcholine) is a potential mediator of the activation of various cell types (Vargaftig et al, 1981;Benveniste & Vargaftig, 1983) including platelets (Benveniste et al, 1975;Cazenave et al, 1979). Doubts were raised concerning the relevance of aggregation of human platelets by Paf-acether, since it has been claimed that the release of ADP (the mediator of the first pathway of aggregation) and/or of arachidonic acid (the mediator of the second pathway; Vargaftig & Zirinis, 1973) fully account for aggregation (Marcus et al, 1981;McManus et al, 1981;Tsien et al, 1982;Chesney et al, 1982;Rao et al, 1982;Ostermann et al, 1983). This is an important problem, since if indeed Paf-acether activates human platelets through aspirin-inhibitable mechanisms (i.e.…”

Section: Introductionmentioning

confidence: 99%

“…Doubts were raised concerning the relevance of aggregation of human platelets by Paf-acether, since it has been claimed that the release of ADP (the mediator of the first pathway of aggregation) and/or of arachidonic acid (the mediator of the second pathway; Vargaftig & Zirinis, 1973) fully account for aggregation (Marcus et al, 1981;McManus et al, 1981;Tsien et al, 1982;Chesney et al, 1982;Rao et al, 1982;Ostermann et al, 1983). This is an important problem, since if indeed Paf-acether activates human platelets through aspirin-inhibitable mechanisms (i.e.…”

Section: Introductionmentioning

confidence: 99%

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Triggering by Paf‐acether and adrenaline of cyclo‐oxygenase‐independent platelet aggregation

Fouque

Vargäftig

1984

British J Pharmacology

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Platelet‐activating factor (Paf‐acether, 1‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphorylcholine) induced full aggregation and a limited release reaction of human platelets in plasma or in blood. Cyclo‐oxygenase inhibition with aspirin only reduced aggregation when induced by threshold amounts of Paf‐acether, whereas higher concentrations surmounted inhibition whether tested in citrated or in heparinized platelet‐rich plasma or blood. Aspirin‐induced inhibition of platelet secretion by Paf‐acether was insurmountable and independent of the anti‐coagulant used. Paf‐acether and adrenaline acted synergistically in inducing aggregation in citrate and in heparin. Aspirin in vitro or after oral ingestion at doses that suppressed aggregation induced by arachidonic acid alone, failed to reduce significantly the synergized aggregation induced by Paf‐acether alone or combined with adrenaline. Twenty‐four hours after the oral ingestion of aspirin, when aggregation by arachidonic acid remained blocked, a slight inhibitory activity on the effect of Paf‐acether noted 4 h after aspirin, had ceased. This was probably accounted for by the synthesis of thromboxane A2 by newly formed platelets, since the in vitro addition of aspirin, or of the thromboxane/endoperoxide receptor inhibitor 13‐azaprostanoic acid caused the 24 h platelets to behave in a manner similar to platelets collected 4 h after aspirin. The α2‐adrenoceptor inhibitor, yohimbine, blocked the direct effect of adrenaline as well as its synergism with Paf‐acether. Since the synergistic effect of Paf‐acether and adrenaline was maintained when thrombin‐degranulated platelets were used, and aspirin remained ineffective against it, it is clear that the augmented platelet responsiveness is not accounted for by the platelet release reaction. Paf‐acether and adrenaline act synergistically and stimulate platelets by cyclo‐oxygenase‐independent mechanisms, which may be relevant in human physiopathological conditions.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Triggering by Paf‐acether and adrenaline of cyclo‐oxygenase‐independent platelet aggregation

Fouque

Vargäftig

1984

British J Pharmacology

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“…et al 1979P. et al , Kelefiotis, D. et al 1988 Ο PAF σε συγκεντρώσεις που δεν προκαλεί συσσώρευση παρουσιάζει συνεργιστική δράση με την αδρεναλίνη και το ADP ( Ostermann, G. et al 1983, Vargaftig, Β.Β. et al 1982.…”

Section: γ) με την επίδραση του Pafunclassified

Μελετη Ενωσεων Με Βιολογικη Δραση Αναλογη Του Paf Και Αναστολεων Του Paf Ζωικης Φυτικης Και Συνθετικης Προελευσης

Αντωνοπουλου¹

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Κωνσταντίνου Αημόπουλου, τον οποίον ευχαριστώ βαθύτατα για τη συμπαράσταση του, για το αμέριστο ενεργό ενδιαφέρον του και για την πολύτιμη βοήθεια του στη διεξαγωγή των πειραμάτων. Ακόμα τον ευχαριστώ θερμά για τη μεγάλη συμβολή του στην τελική εμφάνιση του κειμένου και των σχημάτων της εργασίας αυτής. Το Αιευθυντή του Εργαστηρίου, Καθηγητή κ. Αημήτριο Γαλανό ευχαριστώ για τη δυνατότητα που μου παρείχε να εργαστώ στο εργαστήριο. Τις Επίκουρες Καθηγήτριες του Τμήματος Χημείας κ. Μαίρη Μαυρή και κ. Νάση Σιαφάκα ευχαριστώ για τη συμμετοχή τους στην τριμελή επιτροπή της διδακτορικής διατριβής και για τις διορθώσεις τους στο τελικό κείμενο. Τον Καθηγητή Βιοχημείας κ. Βασίλειο Καπούλα ευχαριστώ θερμά για την επιστημονική του συμπαράσταση. Στο φίλο Λέκτορα του Χαροκόπειου Πανεπιστημίου Αθηνών κ. Νίκο Ανδρικόπονλο οφείλω ένα μεγάλο ευχαριστώ για το συνεχές ενδιαφέρον του στην εξέλιξη της ερευνητικής εργασίας και για την πολύτιμη βοήθεια του στην εκμάθηση της υγρής χρωματογραφίας υψηλής πίεσης.

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Vascular graft‐associated complement activation and leukocyte adhesion in an artificial circulation

Kottke‐Marchant

Anderson

Miller

et al. 1987

J. Biomed. Mater. Res.

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Complement-associated leukocyte adhesion appears to be a consistent in vitro and in vivo finding for many types of polymers; however, very little work has been done on the interaction of leukocytes with vascular graft materials. An in vitro perfusion system was used to study complement and leukocyte activation associated with the following vascular graft materials when tested with human blood: expanded polytetrafluoroethylene (ePTFE), crimped Dacron Bionit (DB) and preclotted Dacron Bionit. A decrease in the total leukocyte concentration with perfusion time was seen for all materials tested, and paralleled leukocyte adhesion to the graft surface as observed by scanning electron microscopy. The most dramatic decrease in leukocyte concentration was observed for the interaction of heparinized whole blood with Dacron. This was due to a selective decrease in neutrophils and monocytes, and was correlated with an increase in both leukocyte adhesiveness and complement activation, as measured by C5a elevation. Inhibiting complement activation by use of the anticoagulant, sodium citrate, curtailed Dacron-induced leukocyte adhesion. Little leukocyte or complement activation was observed for ePTFE or the silicone rubber control regardless of the anticoagulant used.

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Studies on the stimulation of human blood platelets by semisynthetic platelet-activating factor

Cited by 30 publications

References 13 publications

Triggering by Paf‐acether and adrenaline of cyclo‐oxygenase‐independent platelet aggregation

Triggering by Paf‐acether and adrenaline of cyclo‐oxygenase‐independent platelet aggregation

Μελετη Ενωσεων Με Βιολογικη Δραση Αναλογη Του Paf Και Αναστολεων Του Paf Ζωικης Φυτικης Και Συνθετικης Προελευσης

Vascular graft‐associated complement activation and leukocyte adhesion in an artificial circulation

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