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NO is an endogenously produced vasodilator and is largely implicated in hemostatic mechanisms [3–9] while, in tail amputation and heparin-/warfarin-administration models, both the NO-synthase (NOS)-blocker, L-NAME (thought to have a prothrombotic effect) [3] and NOS-substrate, L-arginine [presented with an antithrombotic effect) [3] were little investigated