Activation and Consumption of Hageman Factor in the Anaphylactic Shock of the Rat

Abstract

In the early stages of anaphylactic shock of rats pretreated with Bordetella pertussis vaccine, a prompt and parallel activation of the factor XIIa-dependent intrinsic coagulation, kinin generation, and fibrinolytic acticity was observed. The coagulation studies, the similarity of anaphylactic results with those produced by a single injection of ellagic acid, and the effective inhibition of the anaphylactic and the ellagic acid-induced activation of these pathways by lysozyme all suggest that factor XII itself becomes activated in rat anaphylaxis. As the reaction proceeded, considerable anticoagulant activities emerged, but the bradykinin and the plasminogen activator levels even further increased. During the first 10 min of anaphylactic shock, factor XII was partly consumed and this was prevented by ε-aminocaproic acid infusion. The results show that in pathological conditions such as anaphylaxis there is an intimate in vivo interaction among the three factor Xlla-dependent pathways.

Contact Factors in Health and Disease

“…80 In animal experiments, however, there are some data supporting the activation of Factor XII during anaphylaxis. In rats anaphylaxis was reported to cause a sharp decrease in the levels of Factor XII, as if this factor was activated and in activated, 31 and in rabbits specific IgE antibodies induced a significant reduction of Factors XII, XI, and IX levels. 87 Fifteen minutes after the intra venous administration of bovine serum albumin (BSA) into 3-month-old rabbits producing anti-BSA antibodies only of the IgE class, the titers of Factors XII and XI decreased by 28 and 39%, respectively.…”

Physiological Effects of the Plasma Kallikrein-Kinin System: Roles of the Blood Coagulation Factor XII (Hageman Factor)

“…The findings of these studies may indeed represent the solitary role of FXII in the pathophysiology of stress-related dysfunctional endothelium. Although its activation is not mediated by immune complexes [9], activation of FXII during the initial event in Disseminated Intravascular Coagulopathy (DIC), Rheumatoid Arthritis (RA), inflammation, complement system, and lupus have been described [10][11][12][13]. FXIIa might be a biomarker for endothelial cell activation and early development of endothelial dysfunction in the blood vascular system.…”