Anticoagulant activities of acidic glycosaminoglycans:cooperative action with AT III
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概要
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Heparin is one of the acidic glycosaminoglycans (AGAG). And heparin is being used in the capacity of anticoagulant agent, generally. But heparin dose not have anticoagulant activity by itself at medical dosage. But heparin has only cooperative action with AT III in the sense that heparin increases the anticoagulant activity of AT III at the level of general dosage. Although there is no heparin in peripheral blood and layers of human vessels, but this fact has not been widely known.This paper investigates the cooperative anticoagulant activity of AT III with natural and synthetic AGAG and makes clear the mechanism of the cooperative effect between AT III and AGAG. On the other hand, this paper discusses the meaning of this cooperative anticoagulant mechanism.The following results were obtained.1) The cooperative anticoagulant activities of AT III with different AGAG were compared by heparin cofactor method. It was found that 0.0025mg/ml of heparin had 0.6 antithrombin unit (ATU)/ml of anticoagulant activity by itself. Dermatan sulfate, heparan sulfate and keratan sulfate respectively had 0.2ATU/ml of anticoagulant activity. Also 0.0025mg/ml of synthetic amylopectin sulfate had 8.0ATU/ml and 0.0025mg/ml of synthetic chondroitin polysulfate had 2.6ATU/ml.On the other hand cooperative activity of heparin with AT III produced an increase of 7.9ATU/ml in anticoagulant activity of AT III. This cooperative increase with dermatan sulfate was 5.6ATU/ml. But cooperative actions of synthetic amylopectin sulfate with AT III did not show any increase in anticoagulant activities of AT III (Table 1).2) Continual observations over a time period of 60 minuets on cooperative activities of heparin or dermatan sulfate with AT III showed that reactions between AT III and thrombin were accelerated by adding heparin or dermatan sulfate to AT III. Besides, final anticoagulant activities of AT III with heparin dermatan sulfate were much greater than that of AT III alone (Fig. 1).3) By immunoelectrophoretic investigations, it was observed that each AGAG combined with AT III and the AT III-AGAG complex was made (Fig. 2).4) It was made clear that AT III had allosteric effect, and heparin and dermatan sulfate were allosteric effectors.5) It is suggested that specific molecular structure of AGAG in needed for causing comformation change of AT III.6) This allosteric effect of AT III may imply simultaneous regulation mechanism of extravaso-coagulation and intravaso-anticoagulation.7) In human vessels, dermatan sulfate may be the true allosteric effector on AT III.
- 一般社団法人 日本血栓止血学会の論文
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