Nagai H, Kurimoto Y, Koda A
Microbiol Immunol. 1980;24(7):649-55. doi: 10.1111/j.1348-0421.1980.tb02866.x.
Forssman shock (FS) following the intravenous injection of antisheep erythrocyte antibody into guinea pigs resulted in fatal systemic shock with marked decrease in CH50 values of complement, leucocyte, and platelet counts, and a prolongation of blood coagulation time. In addition, there was an increase in lactate dehydrogenase activity, and decreases in both esterase activity and fibrinogen levels were noted. F(ab')2 of antisheep erythrocyte IgG antibody was not capable of eliciting FS. Cobra venom factor showed a fairly potent inhibition of FS. Leukopenia induced by cytosine arabinoside given intraperitoneally for 5 days had no effect on FS. Colchicine, which decreased the leucocyte count, did not inhibit fatal systemic shock. Administration of heparin or trasyrol did not prevent FS. The present findings demonstrate that FS is inhibited by anticomplementary agents but not by drugs which affect leucocyte and platelet counts, the coagulation system or serum proteases.
给豚鼠静脉注射抗绵羊红细胞抗体后引发的福斯曼休克（FS）会导致致命的全身性休克，伴有补体CH50值显著降低、白细胞和血小板计数减少以及凝血时间延长。此外，乳酸脱氢酶活性增加，酯酶活性和纤维蛋白原水平均降低。抗绵羊红细胞IgG抗体的F(ab')2不能引发FS。眼镜蛇毒因子对FS有相当强的抑制作用。腹腔注射阿糖胞苷5天诱导的白细胞减少对FS没有影响。降低白细胞计数的秋水仙碱不能抑制致命的全身性休克。给予肝素或抑肽酶并不能预防FS。目前的研究结果表明，FS可被抗补体药物抑制，但不受影响白细胞和血小板计数、凝血系统或血清蛋白酶的药物抑制。
