血浆血管性血友病因子的促黏附活性是否会被血小板黏附的生理抑制剂所抵消？
Is the pro-adhesive activity of plasma von Willebrand factor counteracted by a physiological inhibitor of platelet adhesiveness?
作者信息
Porta M, Cagliero E, Kohner E M
出版信息
Clin Sci (Lond). 1982 Feb;62(2):239-42. doi: 10.1042/cs0620239.
PMID:6797774
Abstract
- Abnormal plasma levels of von Willebrand factor are accompanied by abnormal platelet function in some disease states. 2. Platelet retention in glass bead columns, platelet aggregation in vitro, beta-thromboglobulin and 6-oxo-prostaglandin F1 alpha were monitored in six normal male volunteers before and after an acute rise of von Willebrand factor, as induced by the intravenous administration of 1-deamino 8-D-arginine vasopressin (DDAVP). 3. After DDAVP a steady twofold rise of von Willebrand factor occurred. Platelet retention increased by 74% immediately after DDAVP but returned to baseline values within 60-120 min. No consistent changes of the other variables were observed. 4. These results suggest that as yet unidentified mechanism(s) inhibits the pro-adhesive activity of von Willebrand factor.
摘要
- 在某些疾病状态下，血管性血友病因子的血浆水平异常会伴有血小板功能异常。2. 在六名正常男性志愿者静脉注射1-去氨基-8-D-精氨酸加压素（DDAVP）诱导血管性血友病因子急性升高之前和之后，监测玻璃珠柱中的血小板滞留、体外血小板聚集、β-血小板球蛋白和6-氧代前列腺素F1α。3. 注射DDAVP后，血管性血友病因子稳定地升高了两倍。注射DDAVP后，血小板滞留立即增加了74%，但在60-120分钟内恢复到基线值。未观察到其他变量的一致变化。4. 这些结果表明，尚未明确的机制抑制了血管性血友病因子的促黏附活性。
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