Tsai C C, Taichman N S, Pulver W H, Schönbaum E
Am J Pathol. 1973 Aug;72(2):179-200.
Platelets appear to be pathogenetic determinants in the development of lethal Forssman shock, which was provoked in guinea pigs by an intravenous injection of rabbit antiserum to sheep erythrocyte stromata. Within moments, circulating platelets (prelabeled with (14)C-serotonin) were removed from the blood stream and impacted in the lungs, where they liberated (14)C into the tissues. When animals were depleted of platelets prior to the production of shock, they survived for prolonged periods of time or were protected against death. Pretreatment with antiinflammatory compounds capable of inhibiting platelet aggregation and release phenomena had a similar protective influence. It would appear, therefore, that Forssman shock is a convenient and accessible model for investigating the mechanisms whereby platelets mediate immune vascular damage.
血小板似乎是致死性福斯曼休克发展过程中的致病决定因素，该休克是通过给豚鼠静脉注射兔抗绵羊红细胞基质血清诱发的。片刻之内，循环中的血小板（预先用（14）C - 血清素标记）从血流中被清除并聚集在肺部，在那里它们将（14）C释放到组织中。当动物在休克产生前血小板减少时，它们存活时间延长或受到保护免于死亡。用能够抑制血小板聚集和释放现象的抗炎化合物进行预处理具有类似的保护作用。因此，似乎福斯曼休克是研究血小板介导免疫性血管损伤机制的一个方便且可及的模型。
