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Kallikrein-kinin system in chronic subdural haematomas: its roles in vascular permeability and regulation of fibrinolysis and coagulation.
  1. H Fujisawa,
  2. H Ito,
  3. S Kashiwagi,
  4. S Nomura,
  5. M Toyosawa
  1. Department of Neurosurgery, Yamaguchi University School of Medicine, Ube, Japan.


    The kallikrein-kinin system is closely related to both fibrinolysis and coagulation, and bradykinin--the end product of this system--is a powerful mediator which increases vascular permeability. In the present study, to test the hypothesis that the kallikrein-kinin system plays a part in the aetiology of chronic subdural haematomas, components of this system (prekallikrein, high molecular weight kininogen (HMW-kininogen), and bradykinin), and those of the fibrinolytic and coagulation systems were measured at 134 haematoma sites in 119 patients. The activities of prekallikrein and HMW-kininogen in the haematomas were significantly lower than those in the plasma of the patients, and showed a parallel decrease. The bradykinin concentration in the haematomas was significantly higher than that in the plasma. These results indicate activation of the kallikrein-kinin system in chronic subdural haematomas. The activation of both fibrinolysis and coagulation was also shown, and there was a significant correlation between HMW-kininogen and plasminogen, fibrin/fibrinogen degradation products, or platelets in the haematomas. This suggests regulation of fibrinolysis and coagulation by the kallikrein-kinin system or mutual stimulation of these systems. In the outer membrane, perivascular haemorrhage, interstitial oedema, and leucocyte migration were evident microscopically, indicating an increase in vascular permeability. The protein concentration in the haematomas was significantly higher than that in the peripheral blood, indicating plasma exudation from the capillaries in the outer membrane. The activation of the kallikrein-kinin system, by increasing vascular permeability, may cause blood extravasation and plasma exudation from the capillaries into both the outer membrane and the haematoma cavity, resulting in enlargement of the haematoma.

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