Figure 5
Figure 5. DVs directly activate the intrinsic clotting pathway. (A) Clotting time after recalcification of 50% plasma was accelerated significantly in the presence of DVs. Clotting times of the respective buffer controls were taken as the 100% reference in each experiment. Data are expressed as means ± SEM of 5 independent experiments. (B) Isolated DVs dose-dependently enhanced thrombin generation in the prothrombinase assay (n = 4 ± SEM). Controls without DVs did not induce any thrombin generation and are not shown. (C) Procoagulant activity of DVs is sensitive to phospholipase C treatment. Clotting times of 50% citrated plasma were determined after recalcification in the presence of Veronal-buffered saline, Veronal-buffered saline plus PLC, DVs, or DVs after PLC treatment. Clotting time was significantly accelerated in the presence of DVs (*P < .05 vs control). This effect was abolished after PLC treatment (oP < .05). Data are expressed as means ± SD of 3 independent experiments.

DVs directly activate the intrinsic clotting pathway. (A) Clotting time after recalcification of 50% plasma was accelerated significantly in the presence of DVs. Clotting times of the respective buffer controls were taken as the 100% reference in each experiment. Data are expressed as means ± SEM of 5 independent experiments. (B) Isolated DVs dose-dependently enhanced thrombin generation in the prothrombinase assay (n = 4 ± SEM). Controls without DVs did not induce any thrombin generation and are not shown. (C) Procoagulant activity of DVs is sensitive to phospholipase C treatment. Clotting times of 50% citrated plasma were determined after recalcification in the presence of Veronal-buffered saline, Veronal-buffered saline plus PLC, DVs, or DVs after PLC treatment. Clotting time was significantly accelerated in the presence of DVs (*P < .05 vs control). This effect was abolished after PLC treatment (oP < .05). Data are expressed as means ± SD of 3 independent experiments.

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