Figure 1.
Figure 1. Aspirin inhibits platelet NO consumption. (A) Aspirin-treated or -untreated platelets (1 mM, 30 minutes, room temperature) were placed in the chamber of the NO electrode at 0.2 × 109/mL in 500 μL Tyrode buffer containing 1 mM CaCl2 at 37°C. NO (3.8 μM) was added, and decay was monitored, with and without addition of 50 μM arachidonate. Representative trace showing NO consumption by control platelets from one subject, (i) control, (ii) with arachidonate added at arrow. (B) Representative trace showing NO consumption by aspirin-treated platelets from the same subject as in A, (i) control, (ii) with arachidonate added at arrow. (C) Cumulative data on the effect of aspirin treatment on arachidonate-stimulated platelet NO consumption rates (mean ± SEM; n = 3 separate donors; *P < .05, Student unpaired t test).

Aspirin inhibits platelet NO consumption. (A) Aspirin-treated or -untreated platelets (1 mM, 30 minutes, room temperature) were placed in the chamber of the NO electrode at 0.2 × 109/mL in 500 μL Tyrode buffer containing 1 mM CaCl2 at 37°C. NO (3.8 μM) was added, and decay was monitored, with and without addition of 50 μM arachidonate. Representative trace showing NO consumption by control platelets from one subject, (i) control, (ii) with arachidonate added at arrow. (B) Representative trace showing NO consumption by aspirin-treated platelets from the same subject as in A, (i) control, (ii) with arachidonate added at arrow. (C) Cumulative data on the effect of aspirin treatment on arachidonate-stimulated platelet NO consumption rates (mean ± SEM; n = 3 separate donors; *P < .05, Student unpaired t test).

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