Fig. 3.
Fig. 3. Shear-induced platelet aggregation at high shear stress and low shear stress. / Heparinized whole blood was subjected to a shear rate of 3000 s−1 (120 dynes/cm2) for 30 seconds, followed by 150 seconds at 100 s−1 (5 dynes/cm2) in a cone-and-plate viscometer at room temperature. Samples taken before shearing, after 30 seconds at 3000 s−1, and after 180 seconds were immediately fixed in 1% formaldehyde–PBS. Fixed whole blood samples were incubated with anti–CD42a-FITC (anti-GPIX), and the extent of platelet aggregation was determined by flow cytometry. Values are mean ± SEM. *Significant difference from the percentage of platelet aggregation after 30 seconds; P < .05. Control, closed squares; 100 μM A3P5P, closed triangles; 5 μg/mL abciximab, open squares; 0.5 μM ARMX, closed circles; 0.5 μM ARMX + 100 μM A3P5P, closed diamonds.

Shear-induced platelet aggregation at high shear stress and low shear stress.

Heparinized whole blood was subjected to a shear rate of 3000 s−1 (120 dynes/cm2) for 30 seconds, followed by 150 seconds at 100 s−1 (5 dynes/cm2) in a cone-and-plate viscometer at room temperature. Samples taken before shearing, after 30 seconds at 3000 s−1, and after 180 seconds were immediately fixed in 1% formaldehyde–PBS. Fixed whole blood samples were incubated with anti–CD42a-FITC (anti-GPIX), and the extent of platelet aggregation was determined by flow cytometry. Values are mean ± SEM. *Significant difference from the percentage of platelet aggregation after 30 seconds; P < .05. Control, closed squares; 100 μM A3P5P, closed triangles; 5 μg/mL abciximab, open squares; 0.5 μM ARMX, closed circles; 0.5 μM ARMX + 100 μM A3P5P, closed diamonds.

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