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Last Updated: 3 years ago

Possible Interaction: Arachidonic Acid and Epoprostenol

Research Papers that Mention the Interaction

In vitro 9 beta-methyl carbacyclin and epoprostenol inhibited platelet aggregation induced by ADP, collagen, the endoperoxide analogue U46619 and arachidonic acid.
British journal of clinical pharmacology  •  1984  |  View Paper
The studies first demonstrate that a single protein with three … Km of approximately 3.2 microM. Specific upregulation of PGI2 biosynthesis through expression of the engineered … inhibiting platelet aggregation induced by AA in vitro, which creates a great potential for the … new therapeutic interventions for strokes and heart attacks.
Biochemistry  •  2006  |  View Paper
The substance has been shown to modulate arachidonic acid metabolism by enhancing the production and release of prostacyclin and prostaglandin E2 from tissues and whole blood, and inhibiting leukotriene B4 generation in leukocytes.
Seminars in thrombosis and hemostasis  •  1996  |  View Paper
Inhibition occurred in the human cultures when PGI2 formation was elicited with arachidonic acid , ionophore A23187 or thrombin.
Prostaglandins  •  1986  |  View Paper
Treatment of the WPS with prostacyclin (PGI2) or iloprost prior to stimulation by AA resulted in a dose-dependent inhibition of the 5-HT-mediated contraction, due to inhibition of 5-HT release.
Journal of cardiovascular pharmacology  •  1986  |  View Paper
The discovery of prostacyclin has given a new insight into arachidonic acid metabolism and has led to a new hypothesis about mechanisms of haemostasis.
Advances in prostaglandin, thromboxane, and leukotriene research  •  1982  |  View Paper
Administration of arachidonic acid (AA) (45 micrograms) to the system led to a further increase (eight- to ninefold) of PGI2 and yielded marked thromboxane formation (20-25 ng/ml).
The American journal of physiology  •  1981  |  View Paper
The discovery of prostacyclin has given a new insight into arachidonic acid metabolism and has led to a new hypothesis about mechanisms of haemostasis.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences  •  1981  |  View Paper
These labile metabolites of AA antagonize each other: thromboxane A2 is a vasoconstrictor and proaggregatory agent, whereas prostacyclin dilates arteries, prevents platelets from aggregation, and dissipates the preformed platelet clumps.
CRC critical reviews in biochemistry  •  1980  |  View Paper
PGI2 dose dependently inhibits platelet activation induced by adenosine-5′-diphosphate, arachidonic acid , collagen, and low-dose thrombin.
Seminars in cardiothoracic and vascular anesthesia  •  2018  |  View Paper
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