Elsevier

Thrombosis Research

Volume 26, Issue 6, 15 June 1982, Pages 389-400
Thrombosis Research

Paper
A thromboxane synthetase inhibitor reorients endoperoxide metabolism in whole blood towards prostacyclin and prostaglandin E2

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Abstract

During incubation of citrated blood at 37°C the levels of 6-ketoprostaglandin F1α (6-keto PGF1α) and prostaglandin E2 (PGE2) remain constant, but rise markedly within one minute after the addition of collagen, particularly when thromboxane synthetase is blocked. The amount of 6-keto PGF1α formed is dose-dependent for both collagen and the thromboxane synthetase inhibitor (UK-37,248). Moreover, the number of platelets will determine the extent of the 6-keto PGF1α jump, that does not occur when blood is drawn after aspirin ingestion. The production of 6-keto PGF1α in function of time is composed of a fast platelet-related (intercept) and a slower probably leukocyte-dependent contribution (slope). In the absence of UK-37,248 the intercept is 115 ± 85 pg/ml, the slope is 12.9 ± 7.7 pg/min/ml whereas in the presence of the thromboxane synthetase inhibitor they are 411 ± 177 pg/ml and 56.2 ± 25 pg/min/ml respectively. The present findings indicate that a thromboxane synthetase inhibitor, by not only reducing thromboxane A2 production but also enhancing prostacyclin generation when blood is exposed to thrombogenic stimuli such as collagen, should be superior to aspirin as an antithrombotic agent, although possible interference by enhanced PGE2 production should be taken into account.

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