| Popis: |
Platelet aggregation by adenosine 5′-diphosphate (ADP) plays a key role in the development and extension of arterial thrombosis. ADP has also been implicated in vascular smooth muscle cell proliferation leading to restenosis at sites of vascular injury (Crowley et al. 1994). ADP-removing systems infused to animals species with platelet storage pool disease, for example Fawn-Hooded rats lacking ADP in their platelet dense granules, have proven valuable tools to assess the role of ADP in vivo (Born 1985; Maffrand et al. 1988). Specific inhibitors of the ADP activation pathway such as the antiaggregatory thienopyridine compounds ticlopidine and Clopidogrel (Schror 1993) markedly prolong bleeding time and are used clinically as antithrombotic drugs (Verry et al. 1994). Furthermore, a rare congenital bleeding disorder with impairment of ADP-induced platelet aggregation (Cattaneo et al. 1992; Nurden et al. 1995) strikingly resembles the acquired thrombopathy resulting from ticlopidine or Clopidogrel intake (Di Minno et al. 1985; Gachet et al. 1995). Obviously, a better knowledge of the ADP platelet activation pathway is of major importance for the understanding of the physiology of primary hemostasis and for the development of new antithrombotic strategies. |
