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急性炎症发病机制的研究:III. 抗凝剂未能预防热损伤兔耳室中小血栓形成和白细胞黏附反应。

STUDIES ON THE PATHOGENESIS OF ACUTE INFLAMMATION : III. THE FAILURE OF ANTICOAGULANTS TO PREVENT THE LEUCOCYTIC STICKING REACTION AND THE FORMATION OF SMALL THROMBI IN RABBIT EAR CHAMBERS DAMAGED BY HEAT.

机构信息

Division of Infectious Diseases, Departments of Medicine and Microbiology, University of Mississippi, Jackson.

出版信息

J Exp Med. 1961 Sep 30;114(4):535-54. doi: 10.1084/jem.114.4.535.

Abstract

Vigorous anticoagulation with heparin sodium and sodium warfarin singly and in combination did not prevent the margination and endothelial sticking reaction of leucocytes in rabbit ear chambers damaged by heat. The general inflammatory reaction observed in this preparation was similarly uninfluenced by the anticoagulants. An unexpected finding after administration of heparin was the enhanced formation of platelet and fibrin-like thrombi within damaged ear chambers. Sodium warfarin did not induce or prevent this heparin effect. Production of these heparin-associated thrombi was minimized in animals subjected to defibrinogenation in vivo whereas leucocytic sticking was not modified. Although defibrinogenation was not absolute, these experiments represent additional proof that the sticking of white blood cells to vascular endothelium is not causally related to the fibrinogen-fibrin system.

摘要

肝素钠和华法林钠单独或联合应用于兔耳腔热损伤模型,不能预防白细胞的边缘沉积和内皮黏附反应。该模型中的一般炎症反应也不受抗凝剂的影响。肝素治疗后的一个意外发现是,在受损的耳腔中形成了增强的血小板和纤维蛋白样血栓。华法林钠既不能诱导也不能预防肝素的这种作用。体内纤维蛋白原降解的动物体内这些肝素相关血栓的形成最小化,而白细胞黏附则没有改变。尽管纤维蛋白原降解不是绝对的,但这些实验进一步证明,白细胞与血管内皮的黏附与纤维蛋白原-纤维蛋白系统没有因果关系。

相似文献

4
LEUCOCYTIC SECRETIONS.白细胞分泌产物。
J Exp Med. 1922 Nov 30;36(6):645-59. doi: 10.1084/jem.36.6.645.

本文引用的文献

2
Heparin and the formation of white thrombi.肝素与白色血栓的形成。
J Physiol. 1938 Feb 16;92(1):20-31. doi: 10.1113/jphysiol.1938.sp003580.

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