Author + information
- Received February 21, 1984
- Revision received May 8, 1984
- Accepted May 12, 1984
- Published online October 1, 1984.
- Jawahar L. Mehta, MD, FACC1,*,
- Paulette Mehta, MD1,
- Larry Lopez, PharmD1,
- Nancy Ostrowski1 and
- Ernie Aguila, BA1
- ↵*Address for reprints: Jawahar L. Mehta, MD, Department of Medicine, University of Florida, Box J-227, J. Hillis Miller Health Center, Gainesville, Florida 32610.
Small doses of aspirin have been shown to inhibit platelet thromboxane A2 while sparing vascular prostacyclin synthesis. Because leukocytes generate prostacyclin and participate in thrombosis along with platelets, the effects of three different doses of aspirin (40, 325 and 650 mg) on platelet function as well as on endogenous biosynthesis of thromboxane A2 and prostacyclin in whole blood were examined. In normal volunteers given a single 40 mg dose of aspirin, platelet aggregation and adenosine triphosphate release were inhibited for 24 hours. In contrast, platelet function was inhibited for 4 to 7 days in volunteers given 325 or 650 mg of aspirin. Platelet and whole blood generation of thromboxane A2 was inhibited less than 60% by the 40 mg dose, but almost completely by both the 325 and 650 mg doses. Likewise, whole blood generation of prostacyclin was inhibited 70% by the 40 mg dose and over 90% by the larger doses. Inhibition of thromboxane A2 as well as of prostacyclin was evident for 4 days with the 40 mg dose and for 7 days with the larger doses. Decreases in whole blood thromboxane A2 and prostacyclin with any dose of aspirin were of similar magnitude. These data indicate that aspirin in doses of 40 to 650 mg inhibits platelet function and biosynthesis of thromboxane A, and prostacyclin in whole blood in human beings in a dose-dependent fashion.
- Received February 21, 1984.
- Revision received May 8, 1984.
- Accepted May 12, 1984.
- American College of Cardiology Foundation