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. 2012 Nov 21;304(3):C273–C279. doi: 10.1152/ajpcell.00174.2012

Fig. 2.

Fig. 2.

EPA- and DHA-treated platelets show reduced thrombin generation rates and lowered levels of extracellular phosphatidylserine (PS) exposure. A: rate of thrombin formation was determined by measuring absorbance of a thrombin chromogenic substrate as a function of time for vehicle- or EPA/DHA-treated washed platelets incubated with Ca2+, prothrombin, and factor Xa (n = 6). *P < 0.05 vs. vehicle. B: vehicle- or EPA/DHA-treated platelets were stimulated with collagen or vehicle in the presence of Ca2+ and incubated with FITC-labeled annexin V (binds to extracellular PS), and fluorescence was analyzed via flow cytometry. Fluorescence was normalized to the level in vehicle-treated platelets. Significance was calculated using the raw median fluorescence from each sample (n = 4). *P < 0.05 vs. vehicle. C: platelets were incubated with 10, 100, 750, or 1,500 μM EPA/DHA and then stimulated with convulxin (CVX), an agonist for the collagen receptor glycoprotein VI. Fold increase represents average degree of agonist-induced FITC-annexin V labeling compared with nonstimulated platelets (n = 4). *P < 0.05 vs. vehicle. Values are means ± SE.

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