Mori W, Aoki N, Shiga J
Am J Pathol. 1981 Apr;103(1):31-8.
Acute and extensive hepatic cell necrosis was produced experimentally in rabbits by means of the Shwartzman mechanism using adeno- and hepatitis B viruses. The change that occurred in the liver was quite severe, namely, areas of hemorrhagic necrosis of various sizes in gross appearance and lytic-coagulative necrosis with hemorrhage and leukocyte-mononuclear cell infiltration histologically. Thrombi formation was noted in and around the necrotic areas, and it was not unusual to see necrosis of an entire lobe. This seems to be a model, to some extent, for human fulminant hepatitis caused by hepatitis virus infection, and suggested that some nonspecific reaction such as intravascular clotting may also play an important role in causing or complicating acute, severe, and extensive necrosis of the liver in human cases. Heparin administration very effectively prevented such hepatic necrosis, which supports the view that the change we observed in the liver was really the Schwartzman reaction; further, it is reminiscent of the fact that heparin administration is sometimes effective in fulminant hepatitis treatment if given at te appropriate stage of the disease.
通过施瓦茨曼机制,利用腺病毒和乙型肝炎病毒在实验中诱导家兔发生急性广泛性肝细胞坏死。肝脏出现的变化相当严重,大体表现为大小不一的出血性坏死区域,组织学上可见溶解性 - 凝固性坏死伴出血及白细胞 - 单核细胞浸润。在坏死区域及其周围可见血栓形成,整个肝叶坏死也并不罕见。这在某种程度上似乎是人类由肝炎病毒感染引起的暴发性肝炎的一个模型,提示血管内凝血等一些非特异性反应在人类病例中导致肝脏急性、严重和广泛性坏死或使其复杂化方面可能也起重要作用。给予肝素能非常有效地预防这种肝坏死,这支持了我们在肝脏中观察到的变化确实是施瓦茨曼反应的观点;此外,这让人联想到在暴发性肝炎疾病的适当阶段给予肝素治疗有时有效的事实。