Anticoagulants, Antiplatelets, and Thrombolytics (Methods in by Shaker A. Mousa

By Shaker A. Mousa

1This selection of overview articles highlights the newest improvement of antithrombotics and offers confirmed experimental tools for the additional improvement of latest and enhanced anticoagulants. one of the state-of-the-art advancements reviewed are the radical utilization of low molecular weight heparins, such antithrombin brokers because the hirudin, and such antiplatelet medicines because the GPIIb/IIIa inhibitors and ADP receptor antagonists. extra suggestions mentioned comprise aspirin and clopidogrel, the accelerated use of polytherapeutic ways, antiproteases (factors IIa, Xa, and VIIa), tissue issue concentrating on, platelet receptor concentrating on, and antithrombin III modulation.

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By Shaker A. Mousa

1This selection of overview articles highlights the newest improvement of antithrombotics and offers confirmed experimental tools for the additional improvement of latest and enhanced anticoagulants. one of the state-of-the-art advancements reviewed are the radical utilization of low molecular weight heparins, such antithrombin brokers because the hirudin, and such antiplatelet medicines because the GPIIb/IIIa inhibitors and ADP receptor antagonists. extra suggestions mentioned comprise aspirin and clopidogrel, the accelerated use of polytherapeutic ways, antiproteases (factors IIa, Xa, and VIIa), tissue issue concentrating on, platelet receptor concentrating on, and antithrombin III modulation.

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Additional resources for Anticoagulants, Antiplatelets, and Thrombolytics (Methods in Molecular Medicine)

Sample text

Incubate anticoagulated whole blood with platelet antagonist or vehicle (control) at 37°C for 10 min. 2. Place a blood specimen (typically ~500 µL) on the stationary platen of a coneand-plate viscometer maintained at 37°C. 3. Take a small aliquot (~3 µL) from the pre-sheared blood sample (see Note 3), fix it with 1% formaldehyde in D-PBS (~30 µL), and process it as outlined in steps 6–8. 4. Expose the blood specimen, in the presence or absence of a platelet antagonist, to well-defined shear levels (typically 4000 s–1 to induce significant platelet aggregation in the absence of a platelet antagonist) for prescribed periods of time (typically 30–60 s).

4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Anticoagulant solution (sodium citrate, porcine heparin, PPACK). Fluorescently labeled platelet-specific antibody. Dulbecco’s phosphate-buffered saline (D-PBS) (with and without Ca2+/Mg2+). Formaldehyde. Type I collagen, from bovine Achille’s tendon. 5 mol/L glacial acetic acid in water. Glass cover slips (24 × 50 mm; Corning; Corning, NY). , Saginaw, MI). Quinacrine dihydrochloride. Prostaglandin E1 (PGE1) and EGTA. Thrombin. Bovine serum albumin (BSA). 6 mM dextrose).

37, 9–18. CH02,9-20,12pgs 20 9/5/03 10:58 AM Page 20 Iqbal and Mousa 30. Herrmann, H. , Moliterno, D. , Ohman, E. , et al. Facilitation of early percutaneous coronary intervention after reteplase with or without abciximab in acute myocardial infarction: results from the SPEED (GUSTO-4 Pilot) Trial. J. Am. Coll. Cardiol. 36, 1489–1496. 31. Ross, A. , et al. (2001) Randomized comparison of enoxaparin, a low molecular weight heparin, with unfractionated heparin adjunctive to recombinant tissue plasminogen activator thrombolysis and aspirin: second trial of Heparin and Aspirin Reperfusion therapy (HART II).

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