Fig. 1.
Fig. 1. Platelet aggregation induced by increasing shear rates. / (A, B) Heparinized whole blood was subjected to shear rates of 750, 1500, and 3000 s−1 (shear stresses, approximately 30, 60, and 120 dynes/cm2) in a cone-and-plate viscosimeter for 30 seconds at room temperature. Presheared and postsheared samples were fixed in 1% formaldehyde–PBS. Platelets in whole blood samples were labeled with anti–CD42a-FITC (anti-GPIX), and the extent of platelet aggregation was determined by flow cytometry. Values are mean ± SEM. *Significant difference from control; P < .05. (A) Control, closed squares; 10 μM A3P5P, open circles; 100 μM A3P5P, closed triangles; 0.5 μM ARMX, open squares. (B) Control, closed squares; 5 μg/mL abciximab, open circles; 0.5 μM ARMX + 10 μM A3P5P, open triangles; 0.5 μM ARMX + 100 μM A3P5P, closed diamonds.

Platelet aggregation induced by increasing shear rates.

(A, B) Heparinized whole blood was subjected to shear rates of 750, 1500, and 3000 s−1 (shear stresses, approximately 30, 60, and 120 dynes/cm2) in a cone-and-plate viscosimeter for 30 seconds at room temperature. Presheared and postsheared samples were fixed in 1% formaldehyde–PBS. Platelets in whole blood samples were labeled with anti–CD42a-FITC (anti-GPIX), and the extent of platelet aggregation was determined by flow cytometry. Values are mean ± SEM. *Significant difference from control; P < .05. (A) Control, closed squares; 10 μM A3P5P, open circles; 100 μM A3P5P, closed triangles; 0.5 μM ARMX, open squares. (B) Control, closed squares; 5 μg/mL abciximab, open circles; 0.5 μM ARMX + 10 μM A3P5P, open triangles; 0.5 μM ARMX + 100 μM A3P5P, closed diamonds.

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