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In a rabbit model of cerebral artery injury, flurbiprofen, sulphinpyrazone, and magnesium salts effectively suppressed thrombus formation, highlighting potential alternative anti-thrombotic mechanisms.
The ability of potential anti-thrombotic agents to modify platelet-thrombus formation in injured cerebral arteries in the rabbit was tested. Low doses of heparin were without effect, while higher doses produced variable suppression of white body formation but at the expense of bleeding. Aspirin did not inhibit white body formation but another non-steroid anti-inflammatory agent, flurbiprofen was able to do so, as was the anti-gout agent, sulphinpyrazone. Magnesium salts both topically and parenterally, suppressed thrombus formation and increased the concentration of ADP which was required to initiate thrombus production at minor injury sites.
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Adams et al. (1979) studied this question.
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