Fig. 5.
Fig. 5. Effect of Ro 31-8220 and 5-5′-dimethyl-BAPTA on GPVI-mediated platelet aggregation. / Aspirin-treated human platelets were washed and resuspended in Hepes-buffered Tyrode solution. Platelet aggregation in response to different concentrations of convulxin (A) or collagen (B) was measured in the presence of exogenously added fibrinogen (1 mg/mL). Extent of aggregation was measured 210 seconds after the addition of the agonist, without pretreatment of platelets with any agent (●), pretreatment with Ro 31-8220 (10 μM) (○), dimethyl-BAPTA (20 μM) (■), or both Ro 31-8220 and dimethyl-BAPTA (▪). The maximum aggregation extent in the absence of any agent was taken as 100% and the remaining values were normalized to this value. In the case of collagen, extent of aggregation in the presence of SC57101, a fibrinogen receptor antagonist, was taken as zero. Each data point is the mean ± SE of 3 measurements using platelets from different donors.

Effect of Ro 31-8220 and 5-5′-dimethyl-BAPTA on GPVI-mediated platelet aggregation.

Aspirin-treated human platelets were washed and resuspended in Hepes-buffered Tyrode solution. Platelet aggregation in response to different concentrations of convulxin (A) or collagen (B) was measured in the presence of exogenously added fibrinogen (1 mg/mL). Extent of aggregation was measured 210 seconds after the addition of the agonist, without pretreatment of platelets with any agent (●), pretreatment with Ro 31-8220 (10 μM) (○), dimethyl-BAPTA (20 μM) (■), or both Ro 31-8220 and dimethyl-BAPTA (▪). The maximum aggregation extent in the absence of any agent was taken as 100% and the remaining values were normalized to this value. In the case of collagen, extent of aggregation in the presence of SC57101, a fibrinogen receptor antagonist, was taken as zero. Each data point is the mean ± SE of 3 measurements using platelets from different donors.

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