Induction of Disseminated Intravascular Coagulation in the Factor XII-deficient Fowl

Induction of Disseminated Intravascular Coagulation in the Factor XII-deficient Fowl
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因子 XII 缺乏的家禽中弥散性血管内凝血的诱导

DOI:
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发表时间:
1973
影响因子:
6.7
通讯作者:
S. Evensen
S. Evensen
中科院分区:
医学2区
文献类型:
--
作者:
F. Skjørten;S. Evensen

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被引文献

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鸟类天然缺乏负责哺乳动物血浆中接触活化反应的凝血因子。在本研究中,鸡肺检查弥散性血管内凝血(DIC)的证据后,无论是液体或细菌内毒素注射5分钟或4小时。这些物质是哺乳动物DIC的有效引发剂,并且因子XII的活化被认为是其触发效应所必需的。液体注射产生血管内沉积物,具有纤维蛋白的光镜染色特性。然而,这些沉积物具有纯粹的颗粒状超微结构;充分的抗凝剂不能阻止其形成,并且没有伴随的血小板聚集。这表明,存款代表沉淀的血浆蛋白,包括纤维蛋白原。内毒素未能产生临床反应、血管内沉积物或血小板聚集。相反,注射同源组织促凝血酶原激酶的动物死亡,在肺小血管中发现具有纤维蛋白超微结构外观的纤维状材料以及血小板聚集体。抗凝治疗可完全预防这些影响。我们的结论是,液体和内毒素都未能触发DIC的因子XII缺陷的家禽,这表明这些物质依赖于接触活化反应的凝血酶的产生。
Summary Birds are naturally deficient in the coagulation factors responsible for the contact activation reactions in mammalian plasma. In the present study, fowl lungs were examined for evidence of disseminated intravascular coagulation (DIC) 5 min or 4 hours after injection of either Liquoid or bacterial endotoxin. These substances are potent initiators of DIC in mammals, and activation of factor XII is believed to be essential for their triggering effect. Liquoid injection produced intravascular deposits with the light microscopical staining properties of fibrin. However these deposits had a purely granular ultra-structure; their formation was not prevented by adequate anticoagulation, and there was no concomitant thrombocyte aggregation. It is suggested that the deposits represent precipitates of plasma proteins, including fibrinogen. Endotoxin failed to produce clinical reactions, intravascular deposits or thrombocyte aggregates. In contrast, animals injected with homologous tissue thromboplastin died, and fibrillar material with the ultrastructural appearance of fibrin, as well as thrombocyte aggregates were found in small pulmonary vessels. These effects were completely prevented by anticoagulation. We conclude that both Liquoid and endotoxin failed to trigger DIC in the factor XII-deficient fowl, suggesting that these substances depend on the contact activation reactions for the generation of thrombin.