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PGI2 inhibition

Prostacyclin I2 (PGI2) inhibits platelet aggregation and relaxes coronary arteries Like PGE2 and TXA2 it is formed from arachidomc acid via PGH2... [Pg.1082]

As noted above, eicosanoids are involved in thrombosis because TXA2 promotes platelet aggregation and PGI2 inhibits it. Aspirin inhibits platelet COX to produce a mild clotting defect. [Pg.451]

Weis, H.J. and Turitto, V.T. (1979). Prostacyclin (prostaglandin l, PGI2) inhibits platelet adhesion and thrombus formation on subendothelium. Blood, 53, 244-250... [Pg.117]

COX-2 synthesises PGI2 (prostacyclin) and the high incidence of myocardial infarctions with selective COX-2 inhibitors has been attributed to inhibition of COX-2 in vascular tissues. Prostacyclin, made by blood vessel walls, inhibits aggregation of platelets and maintains a balance with thromboxane. Thromboxane, which is released by platelets, promotes clotting. Prostacyclin is synthesised mostly by COX-1, but in humans selective COX-2 inhibition reduces its biosynthesis in vivo. This reduced synthesis may lead to an overactive thromboxane system and increased risk of thromboembolism. [Pg.407]

The widely used platelet inhibitor aspirin or acetylsalicylic acid, by acetylating the enzyme cyclooxygenase, inhibits platelet function by preventing the formation of thromboxane A2 and the synthesis of prostaglandin I2 (PGI2) (68). Aspirin has been used in combination with other antiplatelet agents such as ticlopidine, which inhibits ADP-induced platelet aggregation (69). [Pg.151]

Another metabolite of arachidonic acid is prostacyclin (PGI2). As with TxA2, PGI2 is produced continuously. Synthesized by vascular smooth muscle and endothelial cells, with the endothelium as the predominant source, PGI2 mediates effects that are opposite to those of TxA2. Prostacyclin causes vasodilation and inhibits platelet aggregation and, as a result, makes an important contribution to the antithrombogenic nature of the vascular wall. [Pg.212]

PGI2 Vasodilation, maintenance of patent dnctns arteriosns, inhibition of platelet aggregation, pain sensitization, gastric cytoprotec-tion... [Pg.426]

Gastric ulcer PGE PGI2 has been found to promote healing in gastric ulcer. PGE s are cytoprotective at low doses and inhibit gastric acid secretion at higher doses. [Pg.227]


See other pages where PGI2 inhibition is mentioned: [Pg.155]    [Pg.405]    [Pg.393]    [Pg.453]    [Pg.415]    [Pg.667]    [Pg.422]    [Pg.1441]    [Pg.109]    [Pg.110]    [Pg.546]    [Pg.459]    [Pg.56]    [Pg.155]    [Pg.405]    [Pg.393]    [Pg.453]    [Pg.415]    [Pg.667]    [Pg.422]    [Pg.1441]    [Pg.109]    [Pg.110]    [Pg.546]    [Pg.459]    [Pg.56]    [Pg.155]    [Pg.155]    [Pg.168]    [Pg.169]    [Pg.170]    [Pg.405]    [Pg.193]    [Pg.196]    [Pg.272]    [Pg.61]    [Pg.85]    [Pg.28]    [Pg.311]    [Pg.315]    [Pg.160]    [Pg.49]    [Pg.1432]    [Pg.240]    [Pg.319]    [Pg.437]    [Pg.439]    [Pg.262]    [Pg.263]    [Pg.629]    [Pg.227]    [Pg.9]   
See also in sourсe #XX -- [ Pg.175 , Pg.176 ]




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PGI2

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