Arginine inhibits hemostasis activation

Background: The diagnosis and the therapy of in vivo hemostasis activation is of great clinical importance. Artefactual changes of the hemostasis (i.e ., coagulation or fibrinolysis) in vitro have to be prevented. Usual in vit ro anticoagulation by sodium citrate does not fully inhibit coagulation - o r fibrinolysis - activation. Therefore, there is need for a simple physiolo gic inhibitor of hemostasis activation both in diagnosis and therapy of hem ostasis activation. Methods: Whole blood clotting time (WBCT), prothrombin time (PT), activated partial thromboplastin time (APTT), in vitro bleeding test closure time (IVBT-CT), and whole blood aggregometry (WBA) were determ ined in normal human blood or plasma, supplemented with increasing concentr ations Of L-arginine or guanidine. Results: Arginine in concentrations of 5 -100 mM inhibited the WBCT, PT, APTT, IVBT-CT, and WBA. Arginine (50 mM) re sulted in a two-fold prolongation of WBCT, PT, or IVBT-CT (the anti-epineph rine action is superior to the anti-ADP action), a four-fold prolongation o f APTT or a 60% inhibition of WBA. Conclusion: L-Arginine (or guanidine) in hibited the activation of hemostasis. Arginine might be used as hemostasis stabilizer both in the diagnosis and therapy of hemostasis activation. The usage of arginine as an in vitro hemostasis inhibitor might be indicated in the diagnosis of hemostasis activation, as occuring in pharmacological thr ombolysis or disseminated intravascular coagulation (DIC). The storage of b lood or blood products might be improved by arginine stabilization. The ami no acid (and nitric oxide precursor) L-arginine could be an interesting new pharmacologic agent to inhibit a pathologic hemostasis activation. (C) 200 1 Elsevier Science Ltd. All rights reserved.