PROSTACYCLIN (PGI2) INHIBITS THE FORMATION OF PLATELET THROMBI IN ARTERIOLES AND VENULES OF THE HAMSTER CHEEK POUCH

1 Isolated rings of hamster aorta produced an unstable substance which inhibited platelet aggregation in vitro and had the same characteristics as prostacyclin. 2 Prostacyclin inhibited adenosine diphosphate (ADP)‐induced aggregation of hamster platelets in vitro. 3 The effects of prostacyclin on AD...

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Veröffentlicht in:British journal of pharmacology 1997-02, Vol.120 (S1), p.439-443
Hauptverfasser: HIGGS, E.A., HIGGS, G.A., MONCADA, S., VANE, J.R.
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container_issue S1
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container_title British journal of pharmacology
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creator HIGGS, E.A.
HIGGS, G.A.
MONCADA, S.
VANE, J.R.
description 1 Isolated rings of hamster aorta produced an unstable substance which inhibited platelet aggregation in vitro and had the same characteristics as prostacyclin. 2 Prostacyclin inhibited adenosine diphosphate (ADP)‐induced aggregation of hamster platelets in vitro. 3 The effects of prostacyclin on ADP‐induced platelet thrombi in the microcirculation of the hamster cheek pouch were studied with a television microscope. 4 Prostacyclin caused a dose‐dependent increase in the time of iontophoretic application of ADP which was required to induce platelet thrombi formation and embolization in venules (30 to 40 μm diameter). 5 Prostacyclin caused a dose‐dependent reduction in the total time during which ADP‐induced thrombi were observed following local electrical damage to arterioles (40 to 80 μm diameter). 6 Thrombus formation in venules and arterioles was abolished by 500 ng/ml prostacyclin in the Krebs solution superfusing the hamster cheek pouch. 7 Prostacyclin was approximately twenty times more potent than prostaglandin E1 in preventing thrombus formation in the microcirculation.
doi_str_mv 10.1111/j.1476-5381.1997.tb06831.x
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title PROSTACYCLIN (PGI2) INHIBITS THE FORMATION OF PLATELET THROMBI IN ARTERIOLES AND VENULES OF THE HAMSTER CHEEK POUCH
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