Model 560 ca

Whole blood platelet lumi-aggregometry studies were performed on the citrate tubes at the time of diagnosis and repeated following imatinib therapy in all patients. Platelet aggregation (measured as the increase in impedance) and release were simultaneously measured using a whole blood lumi-aggregometer (Model 560-Ca, Chrono-log Corporation, USA) according to the manufacturer’s instructions. The agonists used and their final concentrations were, in sequence, adenosine diphosphate (ADP; Chrono Par 384, Chrono-log Corporation), 5 µM; arachidonic acid (AA; Chrono Par 390), 0.5 mM; ristocetin (Chrono Par 396), 1.0 mg/mL; and collagen (Chrono Par 385), 2 µg/mL. Platelet function testing on all samples was completed within 2 h of collection. Our laboratory reference ranges for platelet aggregation (ohm) and adenosine triphosphate (ATP) release (nmol) were 10-22 ohm and 0.3-2 nmol for ADP, 10-28 ohm and 0.6-3 nmol for AA, 10-32 ohm and 0.3-2 nmol for collagen, and 3-19 ohm for ristocetin.

The rat blood was removed by cardiac puncture and was collected into tubes containing a 3.8% trisodium citrate (9 : 1 v/v) solution. The rat platelet-rich plasma was prepared by centrifugation at 250 × g for 10 min at room temperature. The platelet-poor plasma was prepared by centrifugation of the pellet at 1500 × g for 10 min at room temperature.
Platelet aggregation was monitored by the turbidimetric method described by Born and Cross [16 (link)], using a platelet lumi-aggregometer (Model 560CA; Chrono-log Corporation, Havertown, PA, USA).
The platelet-rich plasma (400 μl) was incubated at 37°C for 1 min with continuous stirring at 1200 rpm. The aggregation of the platelet-rich plasma was induced using platelet agonists as adenosine diphosphate (ADP) at (0.5 and 1 μM) and collagen at (0.5 and 1 μg/ml) (Sigma-Aldrich). Platelet aggregation was expressed as percentage of aggregation in response to ADP or collagen.