Pathophysiological significance of von Willebrand factor in thrombogenesis
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It has been elucidated that the hemorrhagic diathesis observed in von Willebrand's disease (vWD) is ralated to decrease of von Willebrand factor (vWF). This has led to the speculation that vWF plays physiologically an important role in the initial hemostatic mechanism. vWF in the members of three families with vWD was determined by Weiss method using freshly washed platelets. Through a comparative study made on the bleeding time and platelet retention it was estimated that vWF of at least about 50-60% would be necessary to maintain hemostatic mechanism.Using the same specimen, the determination obtained by Weiss method was compared with the quantitative analysis made by ristocetin induced aggregation using the platelets fixed in 4% paraformaldehyde by Allain method. Results obtained by both methods were found to be comparable.Washed platelets regain the ability for aggregation induced by the final concentration of 1.5mg/ml of ristocetin without plasma in several hours after washing. In addition, the present anthors have observed that the higher concentration of ristocetin (2.5mg/ml) could induce aggregation of washed platelets without plasma even immediately after washing. These observations suggest that platelets have vWF in themselves and it would be released by some mechanism in a lapse of time and also by high concentration of ristocetin.Fixed platelets are stable at least 6 weeks and have no aggregability even by high concentration of ristocetin without plasma. But with plasma ristocetin (1.5-2.5mg/ml) can induce the aggregation of fixed platelets. This aggregation could be observed by naked eyes and by phase contrast microscope. Aggregation of fixed platelets with plasma could be inhibited or reversed by changes in pH. It was also confirmed by us to be inhibited by rabbit antihuman FVIII serum. This is consistent with the results obtained on ristocetin induced aggregation by freshly washed platelets by Howard and by us. It is assumed that even after fixation, vWF receptor of platelets could be maintained, and that some physical force of ristocetin might play an important role on ristocetin induced aggregation. It is considered that the involvement of vWF in initial hemostatic mechanism is energy independent platelet contact with vessel wall.
- 一般社団法人 日本血栓止血学会の論文
一般社団法人 日本血栓止血学会 | 論文
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