A thromboelastography study on the in vitro effects of L-arginine and L-NG-nitro arginine methyl ester on human whole blood coagulation and fibrinolysis

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Abstract
The effects of L-arginine and L-NG-nitro arginine methyl ester (L-NAME) on human blood coagulation and fibrinolysis were studied in vitro using computerized thromboelastography and native whole blood. L-Arginine (8–80 $mUM) prolonged the split point (SP), reaction time (R) and biKoatugulierung time (K); and diminished the angle (α), maximum amplitude (MA) and TEG index. L-NAME (0.5–50 $mUM) shortened SP, R and K and increased α, MA and the TEG index in a concentration-dependent manner. Neither L-arginine nor L-NAME had any effect on clot lysis. SP and R indicate the initiation of fibrin-strand formation, therefore L-arginine delayed, while L-NAME promoted the processes leading to fibrin formation. K and α reflect the rate of clot formation and involve fibrin build-up and platelets. Thus, L-arginine inhibited and L-NAME enhanced the rate of clot formation. MA (clot strength) involves the integrity of fibrin strands and platelet aggregation, and again L-arginine was inhibitory, while L-NAME enhanced this interaction. The TEG index indicates the coagulability of the sample; L-arginine was anticoagulant while L-NAME had procoagulant effects. These results are consistent with the inhibitory effects of NO on platelet function and of the platelet-aggregating properties of NOS inhibitors. In addition, NO may play an inhibitory role in the process leading to fibrin formation and also on the interactions between platelets and fibrin. Such effects may be important when considering the clinical use of drugs that affect the NO-cGMP pathway.

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