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[实验性甲状腺毒症中低凝血酶原血症和低凝血因子原血症的机制]

[Mechanism of hypoprothrombinemia and hypoproconvertinemia in experimental thyrotoxicosis].

作者信息

Petrishchev N N, Kiianov V I

出版信息

Biull Eksp Biol Med. 1975 Jul;80(7):24-6.

PMID:1227641
Abstract

The changes in the thromboelastogram (TEG), the activity and disintegration of prothrombin and proconvertin were studied in experiments on rats with thyrotoxicosis induced by giving thyroidin per os. In marked thyroidin intoxication the majority of TEG indices shifted to hypocoagulation. The most distinct changes were: delayed thrombin formation, an increase in the general coagulation constant, and a decrease in the maximal amplitude. Besides, a decrease of the activity and an increase in prothrombin disintegration (particularly of proconvertin) was observed. It is supposed that increased disintegration of these procoagulants is of great importance in the pathogenesis of hypoprothrombinemia and hypoproconvertinemia in thyrotoxicosis.

摘要

对经口给予甲状腺素诱导的甲状腺毒症大鼠进行实验,研究了血栓弹力图(TEG)的变化、凝血酶原和前转变素的活性及降解情况。在明显的甲状腺素中毒时,大多数TEG指标向低凝状态转变。最明显的变化为:凝血酶形成延迟、总体凝血常数增加以及最大振幅降低。此外,还观察到活性降低以及凝血酶原(尤其是前转变素)降解增加。据推测,这些促凝血剂降解增加在甲状腺毒症患者低凝血酶原血症和低前转变素血症的发病机制中具有重要意义。

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Biull Eksp Biol Med. 1975 Jul;80(7):24-6.
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