ALG在体内对血小板作用的机制。
The mechanism behind the effect of ALG on platelets in vivo.
作者信息
Henricsson A, Husberg B, Bergentz S E
出版信息
Clin Exp Immunol. 1977 Sep;29(3):515-22.
Antilymphocyte globulin (ALG) and antiplatelet globulin (APG) were injected in dogs whose autologous platelets were labelled with 51Cr. APG injection resulted in almost complete and irreversible disappearance of labelled platelets. ALG produced thrombocytopenia of the same degree, but this was to a large extent reversible. After injection of ALG the platelets were reversibly trapped in the lung during the time when platelet count in peripheral blood was low. Such trapping was not seen after administration of APG. This suggests an antiplatelet mechanism of ALG quite different from that of APG. Platelet-absorbed ALG and non-platelet-absorbed ALG produced thrombocytopenia of the same degree and pattern, making it less likely that the thrombocytopenia was caused by specific platelet antibodies. Also platelet-absorbed APG induced thrombocytopenia, but this was reversible and 'ALG-like'. The mechanism behind the platelet reaction after an ALG injection is well explained in terms of complement C3 adherence and/or Fc receptor-induced aggregation.
将抗淋巴细胞球蛋白（ALG）和抗血小板球蛋白（APG）注射到自体血小板用51Cr标记的犬体内。注射APG导致标记血小板几乎完全且不可逆地消失。注射ALG产生同等程度的血小板减少，但在很大程度上这是可逆的。注射ALG后，在周围血液中血小板计数较低的时间段内，血小板可逆性地滞留在肺部。注射APG后未观察到这种滞留现象。这表明ALG的抗血小板机制与APG的截然不同。血小板吸附的ALG和未被血小板吸附的ALG产生同等程度和模式的血小板减少，使得血小板减少由特异性血小板抗体引起的可能性降低。同样，血小板吸附的APG也诱导血小板减少，但这是可逆的且“类似ALG”。根据补体C3黏附及/或Fc受体诱导的聚集，能很好地解释注射ALG后血小板反应背后的机制。
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