In rats intravenous aspirin was only slightly more effective an inhibitor of platelet thrombioxane B2 (TxB2) than of aorta 6-keto-prostaglandin (PGF)(1α) generation (1.9 versus 2.1 mg/kg). In contrast, oral aspirin was about five times more effective on platelet than on aorta cyclooxygenase activity. The 'biochemical selectivity' of aspirin as an inhibitor of platelet and vascular cyclooxygenase thus was not apparent after intravenous administration of the drug. However, this could be achieved by relatively low doses of oral (or intraduodenal) aspirin, on account of 'presystemic' acetylation of platelet cyclooxygenase. Even in this condition, though, aspirin selectively was relative to 'systemic' peripheral vessels but not to the vessels of the enterohepatic circulation. Indeed after an oral or intraduodenal dose of 5 mg/kg aspirin, generation of portal vein 6-keto-PGF(1α) was inhibited to much the same extent as platelet TxB2, while inferior vena cava 6-keto-PGF(1α) formation was spared.
|Number of pages||4|
|Journal||Journal of Clinical Investigation|
|Publication status||Published - 1986|
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