Abstract
In the last decade, aspirin has been examined for its efficacy as a blood platelet anti-aggregatory agent in the prevention of secondary myocardial infarction and transient cerebral ischemia. The anti-aggregatory effect of aspirin is due to its inhibition of the enzyme cylcooxygenase in platelets by irreversible acetylation. However, inhibition of this enzyme in the blood vessel wall stimulates platelet aggregation (1). These two opposing effects of aspirin are concentration-dependent, and it has been hypothesized that a narrow range of aspirin plasma concentrations, or areas under the aspirin concentration-time curve (AUC), is required to produce optimal therapeutic effects (1). In view of the more than threefold variation in the AUC’s following oral administration of aspirin in humans (2), it is necessary to establish the factors which determine the systemic availability of unhydrolyzed aspirin. In this study, the pharmacokinetics of aspirin in rats, the hydrolysis of aspirin by rat and human blood, and the correlation betweenin vivo and whole blood hydrolysis of aspirin were investigated.
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