内因性線溶に関する研究 : 活性化と阻害について
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The activation of coagulation Facor XII results in initiation of the intrinsic fibrinolysis. This study was carried out to clarify what promoting and inhibitory factors are related to the process. (1) Promotion (1) In vitro : The fibrionlytic activities were determined by the contact activation of Factor XIIH with four reagents, kaolin, dextran sulphate, ellagic acid and celite. Kaolin showed the strongest effect on increasing in fibrinolysis, which was caused via prekallikrein, namely Factor XII dependent pathway. Though the potency of dextran sulphate to activate prekallikrein was weak, but it enhanced the fibrinolysis independently of Factor XII. (2) In vivo : No contact activating reagent to use in man was available, so any experiment was not done. (2) Inhibition (1) In vitro: It is known that contact factors (Factor XII, Factor XI, prekallikrein and high molecular weight kininogen as cofactors) are under the regulation of C1-inhibitor. To investigate the role of C1-inhibitor in regulation of the intrinsic fibrinolysis, normal healthy subjects and a patient of hereditary angioneurotic edema were examined. By the innactivation of C1-inhibitor, using its blocking reagent, flufenamate, normal plasma showed an increase in fibrinolysis. In plasma of a patient of hereditary angioneurotic edema, conversion of prekallikrein to kallikrein was easily occurred and the fibrinolytic activity was very high with or without activating reagents. (2) In vivo: At the point of view that C1-inhibitor regulates the intrinsic fibrinolysis, flufenamate was administrated in three healthy subjects. They showed an enhancement of fibrinolysis and prekallikrein activation by the administration. It is the first report to recognize the manifestation of the intrinsic fibrinolysis in vivo, by the method of innactivation of C1-inhibitor. It is suggested that Factor XII plays an important role in the initiation of rather the fibrinolytic system than the coagulation system.
- 北海道医療大学の論文
- 1992-06-30
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