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血小板、阿瑟斯型反应与炎症介质。

Platelets, Arthus-type reactions and inflammatory mediators.

作者信息

Ubatuba F B, Ferreira S H

出版信息

Agents Actions. 1976 Jul;6(4):483-9. doi: 10.1007/BF01973264.

Abstract

The release of inflammatory mediators and the appearance of necrohaemorrhagic lesions induced by subcutaneous implantation of sponges containing antiplatelet serum globulins were studied in control and thrombocyto-penic rats. In thrombocytopenic animals, antiplatelet globulins caused a greater release of prostaglanding-like material and 5-hydroxytryptamine as well as larger inflammatory lesions. Thus, platelet integrity is not necessary for the induction of lesions by antiplatelet globulins and the mediators in the sponge exudates must have originated from leucocytes or damaged tissues. Mast cells seem not to be involved in the production of 5-hydroxytryptamine in this inflammatory reaction. It is suggested that in idiopathic thrombocytopenic purpura (ITP) an Arthus-type hypersensitivity reaction, rather than the thrombocytopenia itself, is the cause of the vascular lesions and their manifestations.

摘要

在对照大鼠和血小板减少的大鼠中,研究了皮下植入含有抗血小板血清球蛋白的海绵所诱导的炎症介质释放以及坏死性出血性病变的出现情况。在血小板减少的动物中,抗血小板球蛋白导致了更多类前列腺素物质和5-羟色胺的释放,以及更大的炎症病变。因此,血小板完整性对于抗血小板球蛋白诱导病变并非必要,海绵渗出物中的介质必定源自白细胞或受损组织。肥大细胞似乎未参与这种炎症反应中5-羟色胺的产生。有人提出,在特发性血小板减少性紫癜(ITP)中,阿瑟斯型超敏反应而非血小板减少本身,是血管病变及其表现的原因。

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