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<p>aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance.  However, prostacyclin concentrations recover much faster than thromboxane levels, so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of prostaglandins predominates as they are regenerated). This is explained by understanding the cells that produce each molecule, TXA<sub>2</sub> and PGI<sub>2</sub>. Since PGI<sub>2</sub> is primarily produced in a nucleated endothelial</p><p>
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