2,3-Diphosphoglycerate (2,3-DPG) may inhibit the platelet release reaction and the irreversible aggregation of human blood platelets induced by adenosine diphosphate, epinephrine, or norepinephrine. The effects of 2,3-DPG on platelet aggregation were more pronounced in cases with low hematocrit (less than 30 percent). Dipyridamole and vincaminor potentiated the antiaggregating effect of 2,3-DPG. Erythocytes (10-3 to 10-4 per microliter) exhibited a similar antiaggregating effect, especially when secured from anemic patients.
In in vitro studies, aspirin inhibited the lytic activity of streptokinase (SK), urokinase (UK), plasmin, and of euglobulins prepared from normal and Hageman deficient human plasmas. Aspirin also inhibited the generation of activator activity in the plasminoplastin generation test assay. This anti-fibrinolytic effect of aspirin was not due to its acid pH. Chicken plasma being deficient in Hageman factor and in proactivator exerted also a very potent anti-SK and anti-UK effect.
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