Key result
Inhibition of prostaglandin formation or TXA2-receptor blockade significantly altered embolization duration and number in rabbit arterioles more than in venules.
Prostaglandins play a more important role in thromboembolism in arterioles than in venules, suggesting a difference in prostaglandin synthetic capacity between arteriolar and venular endothelium.
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Prostaglandin inhibition effects differ by vessel type in rabbit model; leaves open targeted antithrombotic research in human arterial versus venous disease.
The involvement of prostaglandins in thromboembolic processes, as induced by wall puncture, was studied in rabbit mesenteric arterioles and venules using intravital videomicroscopy. Inhibition of prostaglandin formation with aspirin (100 mg/kg, i.v.) significantly increased in arterioles duration of embolization (from 91 to 200 s) and number of emboli produced (from 4 to 8.5 per vessel), while rate of embolus production was not influenced. In venules, aspirin only influenced embolization rate (a significant decrease from one embolus/14 s to one/23 s). Specific blockade of TXA2-receptors by sulotroban (30 mg/kg, i.v.) only influenced the arteriolar reaction: it significantly decreased embolization duration (from 560 to 218 s) and number of emboli produced (from 23 to 10 emboli per vessel), without affecting embolization rate. These findings indicate that both platelet activating and inhibiting prostaglandins play a more important role in thromboembolism in arterioles than in venules; this suggests a difference in prostaglandin synthetic capacity between arteriolar and venular endothelium.
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Egbrink et al. (1993) studied Thromboembolic processes. Aspirin and Sulotroban vs. Baseline/control was evaluated on Duration of embolization, number of emboli produced, and rate of embolus production. Inhibition of prostaglandin formation or TXA2-receptor blockade significantly altered embolization duration and number in rabbit arterioles more than in venules.
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