Dose-Related Kinetics of Aspirin
- 8 November 1984
- journal article
- research article
- Published by Massachusetts Medical Society in New England Journal of Medicine
- Vol. 311 (19) , 1206-1211
- https://doi.org/10.1056/nejm198411083111902
Abstract
When aspirin is administered by mouth in low doses, poor systemic bioavailability may contribute to its apparent dose-related "selective inhibition" of THROMBOXANE A2 formation. Systemic bioavailability of orally administered aspirin is necessary to inhibit prostacyclin synthesis by systemic vascular endothelium, whereas cumulative inhibition of thromboxane A2 formation by platelets may occur in the presystemic (portal) circulation.This publication has 31 references indexed in Scilit:
- Increased Prostacyclin Biosynthesis in Patients with Severe Atherosclerosis and Platelet ActivationNew England Journal of Medicine, 1984
- Differential Inhibition by Aspirin of Vascular and Platelet Prostaglandin Synthesis in Atherosclerotic PatientsNew England Journal of Medicine, 1983
- Selective Cumulative Inhibition of Platelet Thromboxane Production by Low-dose Aspirin in Healthy SubjectsJournal of Clinical Investigation, 1982
- Inhibition of Prostacyclin and Platelet Thromboxane A2after Low-Dose AspirinNew England Journal of Medicine, 1981
- Pharmacokinetic analysis and calculations using a program for the minicalculator TI-59International Journal of Bio-Medical Computing, 1981
- Cultured human skin fibroblasts and arterial cells produce a labile platelet-inhibitory prostaglandinBiochemical and Biophysical Research Communications, 1977
- The mechanism of the effect of aspirin on human platelets. I. Acetylation of a particulate fraction protein.Journal of Clinical Investigation, 1975
- Absorption Kinetics of Aspirin in Man follow Oral Administration of an Aqueous SolutionJournal of Pharmaceutical Sciences, 1972
- Hydrolysis of Aspirin by Rat Small IntestineJournal of Pharmaceutical Sciences, 1968
- Individual Comparisons by Ranking MethodsBiometrics Bulletin, 1945