Pinckard R N, Tanigawa C, Halonen M
J Immunol. 1975 Aug;115(2):525-32.
Intravenous administration of BSA into 3-month-old rabbits producing detectable anti-BSA antibody only of the IgE class of immunoglobulin induced a variety of intravascular blood coagulation alterations observed in the plasma 15 min after antigen challenge included: a) the intravascular consumption of intrinsic blood coagulation factors XII, XI, and IX and possibly the reduction in clottable fibrinogen; b) a significant prolongation of the activated partial thromboplastin time but not the prothrombin time; and c) the production of an inhibitor affecting the last stage of blood coagulation. The observed blood coagulation alterations were not caused by the manipulative procedures utilized, the presence of anti-BSA, IgG or IgM antibody, histamine-induced alterations in the vascular endothelium or the development of hypotensive shock. It is proposed that specific IgE antibody can induce directly or indirectly the activation of intrinsic blood coagulation in vivo.
给3个月大的兔子静脉注射牛血清白蛋白(BSA),仅产生可检测到的免疫球蛋白IgE类抗BSA抗体,在抗原攻击后15分钟在血浆中观察到多种血管内血液凝固改变,包括:a)内源性血液凝固因子XII、XI和IX的血管内消耗,以及可能的可凝固纤维蛋白原减少;b)活化部分凝血活酶时间显著延长,但凝血酶原时间未延长;c)产生一种影响血液凝固最后阶段的抑制剂。观察到的血液凝固改变不是由所采用的操作程序、抗BSA、IgG或IgM抗体的存在、组胺诱导的血管内皮改变或低血压休克的发生引起的。有人提出,特异性IgE抗体可直接或间接诱导体内内源性血液凝固的激活。