Thromb Haemost 1966; 16(01/02): 207-217
DOI: 10.1055/s-0038-1655638
Originalarbeiten — Original Articles — Travaux Originaux
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The Role of HF (Factor XII) in the Pathogenesis of the Thrombolytic State Induced by Venous Occlusion[*]

S. G Iatridis
1   Department of Medicine, Athena Clinic, Athenai, Greece
2   Department of Physiology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, U.S.A.
,
P. G Iatridis
1   Department of Medicine, Athena Clinic, Athenai, Greece
2   Department of Physiology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, U.S.A.
,
J. H Ferguson
1   Department of Medicine, Athena Clinic, Athenai, Greece
2   Department of Physiology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, U.S.A.
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Publikationsdatum:
26. Juni 2018 (online)

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Summary

The effect of venous occlusion of the forearm on clotting and fibrinolysis was studied on 17 normal subjects. A post-occlusion increase in AHF (factor (VIII) and HF (factor XII) was noted. Fibrinolytic activity, as measured by euglobulin lysis time, plasma plate method, unheated fibrin plate method and plasminoplastin generation test, increased significantly in most of the subjects. A plasma lysokinase (indirect activator) seems to preponderate; this was also accompanied by some plasminoplastin (direct activator) activity. Low concentrations of ε-ACA and ATPase had an inhibitory effect upon the increased lytic activity. The data suggest that the post-occlusion lytic activity which was characterized to be of the lysokinase-type was intimately related to HF (factor XII).

* This study was aided by USPHS Research Grant No HE-01510, and NIH Institution Research Grant HE-06350 for Thrombosis Research.