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Experimental studies on activation of the kininogenic system after exclusion of the hepatic circulation.

Levels of kininogen and kallikrein activity were studied in the plasma of rabbits with ligated hepatic blood vessels. Ligation of hepatic veins and arteries arrested visceral circulation in the animals and produced symptoms of shock and death of the animals. Ligation of the superior mesenteric artery at the same time prevented these symptoms, creating an experimental model of exclusion of the liver. Fibrinolytic activation of the kininogenic system by intravenous injection of xanthinol nicotinate (Sadamin, Polfa) in rabbits with excluded hepatic blood circulation caused a rise in kallikrein activity and transient drop in levels of kininogen. Return to normal of kininogen levels in the animals with excluded liver indicated that the process of restoration of kininogen deficiency in the blood is a complex one, independent of direct kininogen synthesis in the liver or its release from the liver.