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The role of kininogenases, kinin formation and kininogenase inhibition in post traumatic shock and related conditions

Kininogenasen, Kininbildung und Kininogenasen-Hemmung beim posttraumatischen Schock und verwandten Krankheitszuständen

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Zusammenfassung

Seit langem wird angenommen, daß das Kinin-System an den pathophysiologischen Vorgängen nach Traumata, besonders bei Blutdruck-Veränderungen und bei entzündlichen Reaktionen, eine Rolle spielt. Jüngere Forschungsergebnisse machen es notwendig, diese Ansicht neu zu überdenken. Wir müssen heute zwischen zwei Kinin-Systemen unterscheiden, 1. dem Plasma-Kallikrein-HMW-Kininogen-Kinin-System, welches neben der Kinin-Bildung eine wesentliche Rolle bei der Hageman-Faktor-Aktivierung, in der Geinnung und in der Fibrinolyse spielt; 2. dem Drüsen- und Gewebs-Kallikrein-LMW-Kininogen-Kinin-System, dessen Funktion nach unserem heutigen Wissen in erster Linie die Kinin-Bildung ist.

Kinine üben verschiedenartige Wirkungen aus. Durch eine Beeinflussung der Angiotensin II-Bildung können Kinine zur Blutdruck-Regulation beitragen. Durch eine Verstärkung der zellulären Glukoseaufnahme und/oder des Glukose-Stoffwechsels nehmen sie zum Teil an der Regulation des Energiestoffwechsels teil. In posttraumatischen Zuständen geht dem Tod ein starker Schwund der verschiedenen Faktoren des Systems voraus, verbunden mit einem fast vollständigen Verlust der Kininbildungsfähigkeit. Schweregrad und zeitlicher Verlauf dieser Phänomene legen nahe, einen frühzeitigen Einsatz direkter (Trasylol) oder indirekter (Heparin, Corticosteroide) Proteinasen-Inhibition, wenn notwendig gemeinsam mit einem Ersatz der verbrauchten Faktoren, in Erwägung zu ziehen.

Summary

The kinin system has for a long time been considered to play a role in the pathophysiology of trauma, particularly in blood pressure changes and in inflammatory effects. Recent findings necessitate a revision of this view. It is now necessary to differentiate between two kinin systems: 1. the plasma kallikrein-HMW kininogen-kinin-system, which besides forming kinin acts decisively in Hageman Factor activation, clotting and fibrinolysis; 2. the glandular and tissue kallikrein-LMW kininogen-kinin-system which is to our present day knowledge primarily involved in kinin formation. Kinins exert a variety of actions. By interfering with angiotensin II formation, kinins may contribute to blood pressure regulation. By enhancing cellular glucose uptake and/or metabolism, they regulate partly energy production. In post traumatic states death is preceded by a severe depletion of various factors of the system and an almost total loss of kinin forming capacity. Severity and time course of these phenomena suggest that early institution of direct (Trasylol) or indirect (heparins, cortocosteroids) proteinase inhibition, and if necessary a replacement of the lost factors, should be considered.

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Im Gedenken an Emil Karl Frey 27. Juli 1888 — 6. August 1977

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Haberland, G.L. The role of kininogenases, kinin formation and kininogenase inhibition in post traumatic shock and related conditions. Klin Wochenschr 56, 325–331 (1978). https://doi.org/10.1007/BF01477391

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