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DOI: 10.1055/s-0038-1655455
The Significance of the Hageman-Factor for the Effect of Wettable Surface on Thrombocytes[*]
Publication History
Publication Date:
21 June 2018 (online)
Summary
1. Disintegration of thrombocytes through contact with wettable surfaces — precipitated in the glass rotator in the form of platelet agglomeration — demands the presence of the Hageman-factor, prothrombin and the fibrinogen on the surface of the thrombocytes.
2. For the precipitation of platelet-agglomeration and -disintegration through contact with glass, activation of the complete preliminary phase of blood coagulation is not essential. The process also takes place in the absence of factors V, VIII, IX and X and possibly also without the influence of PTA.
3. On the basis of the present results it can therefore be assumed that disintegration of the thrombocytes through wettable surfaces is brought about by activation of the Hageman-factor on wettable surfaces alone. The activated Hageman-factor probably reacts directly with prothrombin, which leads to sufficient activation of thrombin to cause an increase in adhesiveness and agglomeration of the thrombocytes.
4. This especial thrombocyte disintegration sequence may proceed directly or indirectly. Calcium ions are not essential to either form. Herein lies the fundamental difference to the activation of factor IX through glass contact. Here the direct mechanism does not require calcium ions, whereas these are indispensable for indirect activation.
5. For the activation of the intrinsic system of the plasma, PTA as an intermediary product is most probably indispensable, whereas this is not the case for the precipitation of platelet disintegration through glass contact.
6. The reason why factor IX is not essential to the precipitation of platelet disintegration may be either that the process requires only traces of thrombin, or that disintegration of the platelets is induced already by intermediary products. The precipitation of this sequence through slightest traces of thrombin could be explained by the fact that the lack of antithrombin on the surface of the thrombocytes and the presence of platelet factors 2 and 4 exert a thrombin protecting and thrombin potentiating effect.
The observation that platelet disintegration through contact activation with glass surfaces takes place even in the presence of heparin does not contradict the assumption that this process is brought about via thrombin. Although complete activation of the preliminary phase is prevented, the Hageman-principle is nevertheless activated through surface contact and the larger distance between activated surface and intact platelets is bridged over by the fact that the activated principle is not influenced through the heparin milieu. As soon as it reaches the platelet surface, it can, on account of the thrombin protecting effect, react directly with prothrombin.
8. The results of our investigations suggest that, in extremely severe cases of hepatic cirrhosis, the case of the regularly observed disturbance in platelet function (agglomeration, adhesion, retraction of the thrombocytes and rotation thrombelastography) are due, or partly due, to a significant deficiency of the Hageman-factor.
We wish to express our thanks to the Deutsche Forschungsgemeinschaft, Bad Godesberg, for their support in our investigations.
* Dedicated to Prof. Dr. F. Hoff on the occasion of his 65th birthday.