English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Prostacyclin and thromboxane A2, two of the physiologically most important end products of arachidonic acid metabolism, represent a basic control system which modulates platelet function. Decreased vascular prostacyclin is believed to play a role in the increased thrombotic tendency associated with various clinical diseases including diabetes and atherosclerosis. Compounds which either enhance the formation or release of prostacyclin or potentiate the activity of low levels of prostacyclin may be therapeutically useful in ameliorating this associated pathology. We have studied various inhibitors of platelet aggregation for their ability to potentiate the activity of low levels of prostacyclin both in vitro and in an in vivo model of experimental thrombosis. Anagrelide, aspirin, dipyridamole, sulfinpyrazone and ticlopidine all demonstrated interaction with prostacyclin in vitro against collagen-induced platelet aggregation. More limited interactions were observed against ADP-induced aggregation. Using isobolographic analysis most combinations demonstrated additive interaction. However, pronounced supra-additive interaction was observed vs. both aggregating agents in the case of prostacyclin (0.1-1 ng/ml) - anagrelide (8-90 ng/ml) combinations. Dramatic enhancement of the effects of prostacyclin on biolaser-induced thrombosis was also seen in anagrelide (0.5 mg/kg po) pretreated animals. Other inhibitors of platelet aggregation used in combination with prostacyclin produced less spectacular results. These findings suggest that aside from inherent antiaggregatory and antithrombotic activity, certain platelet active drugs may produce equally important effects by virtue of their ability to interact with prostacyclin in a clinically beneficial manner.

The Interaction Of Platelet Active Drugs With Prostacyclin In Vitro And Against Biolaser Induced Intravascular Thrombosis