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急性低血糖后人体凝血因子VIII活性增加:通过肾上腺素能机制介导。

Increase in coagulation factor VIII activity in man following acute hypoglycaemia: mediation via an adrenergic mechanism.

作者信息

Corrall R J, Webber R J, Frier B M

出版信息

Br J Haematol. 1980 Feb;44(2):301-5. doi: 10.1111/j.1365-2141.1980.tb01212.x.

Abstract

Coagulation factor VIII activity has been assayed in nine normal volunteers before and after acute hypoglycaemia. In all subjects there was a rise in activity with a mean increment of 96%. Control studies using saline failed to demonstrate any change. In four subjects with pre-ganglionic sympathetctomy no increase in activity was observed. In the normal subjects the increase was blocked by propranolol but not by metoprolol, indicating mediation via beta2 receptors.

摘要

在九名正常志愿者身上,对急性低血糖前后的凝血因子VIII活性进行了测定。在所有受试者中,活性均有升高,平均增幅为96%。使用生理盐水的对照研究未显示出任何变化。在四名进行了节前交感神经切除术的受试者中,未观察到活性增加。在正常受试者中,普萘洛尔可阻断这种增加,但美托洛尔则不能,这表明是通过β2受体介导的。

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