Baker D C, Green R A
Vet Pathol. 1987 Jan;24(1):62-70. doi: 10.1177/030098588702400111.
Twelve New Zealand white rabbits were intoxicated with aflatoxin B1. Most rabbits developed a coagulation defect near the time of death. Immediately prior to death there were significant decreases in factors V, VII, and VIII coagulant activities and fibrinogen concentration without a change in plasma fibrin(ogen) degradation product concentration, platelet number, and detectable plasma fibrin monomers. Microscopic evidence of disseminated intravascular coagulation was present in one rabbit with marked, diffuse hepatic necrosis. Terminal serum albumin concentration was significantly correlated to plasma factors V and VII activities and fibrinogen concentration. The coagulation defect of aflatoxicosis is primarily due to diminished hepatic synthesis of coagulation factors except when hepatic necrosis is severe enough to initiate intravascular coagulation and consumption of coagulation factors.
十二只新西兰白兔被黄曲霉毒素B1中毒。大多数兔子在死亡时出现凝血缺陷。死亡前，凝血因子V、VII和VIII的凝血活性以及纤维蛋白原浓度显著降低，而血浆纤维蛋白（原）降解产物浓度、血小板数量和可检测到的血浆纤维蛋白单体无变化。一只伴有明显弥漫性肝坏死的兔子存在弥散性血管内凝血的微观证据。终末期血清白蛋白浓度与血浆凝血因子V和VII活性以及纤维蛋白原浓度显著相关。黄曲霉毒素中毒的凝血缺陷主要是由于肝脏凝血因子合成减少，除非肝坏死严重到足以引发血管内凝血和凝血因子消耗。
