When aspirin is administered by mouth in low doses, poor systemic bioavailability may
contribute to its apparent dose-related" selective inhibition" of THROMBOXANE A2 …

The current dispute over the effects of" low" vs" high" doses of aspirin should take into
consideration the pharmacokinetics of this drug. In fact, different pharmaceutical …

To assess the pharmacologic effects of aspirin on endogenous prostacyclin and
thromboxane biosynthesis, 2, 3-dinor-6-keto PGF1 alpha (PGI-M) and 2, 3-dinor …

Background. The antithrombotic efficacy of aspirin is attributed to its inhibition of the enzyme
prostaglandin G/H synthase, which is necessary for the formation of thromboxane A2 in …

Aspirin inhibits platelet function by permanently acetylating the cyclooxygenase that forms
prostaglandins. We determined the sensitivity of platelets to aspirin in normal subjects by …

Acetylation of platelet cyclooxygenase by oral aspirin is dose dependent and cumulative
with repeated administration. However, no single dose of aspirin has been found to be …

To compare the inhibitory effects of aspirin on prostaglandin synthesized by vessel walls
and platelets, we obtained vein segments from five subjects before they were given 150 or …

Aspirin (acetylsalicylic acid) inhibits platelet prostaglandin synthesis and the ADP-and
collagen-induced platelet release reaction. The mechanism of the inhibitory effect is …

Aspirin and indomethacin do interact with the same site on cyclo-oxygenase. This
suggestion is based on in vitro studies on ram seminal vesicles and in vivo drug interaction …

The purpose of this study was to compare the effects of low-to-high doses of aspirin on
platelet aggregability determined by different methods and on the metabolism of …