Effect of cyclo-oxygenase inhibition on the vWF-induced [Ca²⁺]_i signal and thromboxane A₂ production. Human platelets (50,000 cells/μL, loaded with Fura-PE3) were preincubated (5 minutes at 37°C) with 0.1% dimethylsulfoxide (vehicle) or 0.2 mmol/L aspirin. The platelets were then stimulated at 37°C by 1 mg/mL ristocetin and 5 μg/mL multimeric human vWF in the presence of 1 mmol/L CaCl₂. Parallel control studies were undertaken with 1 mg/mL ristocetin alone. (A) The results from a typical one of nine such studies are shown. The solid trace denotes the vWF-induced [Ca²⁺]_isignal in vehicle-treated platelets, and the dotted trace that after aspirin treatment. (B) The amplitude of the vWF-induced [Ca²⁺]_i increment, relative to ristocetin alone, in the whole set of studies is presented as a Tukey box plot. (C) Thromboxane A₂ production was assessed in parallel. The vWF-induced increment in thromboxane A₂ production, relative to ristocetin alone (typically, 0.3 ng), is displayed as an analogous Tukey box plot. The hatched bars in panels B and C summarize data for platelets preincubated with vehicle and the open bars data for aspirin-treated platelets.