Yoder M C, Egler J M, Yudkoff M, Chatten J, Douglas S D, Polin R A
Infect Immun. 1985 Jan;47(1):329-31. doi: 10.1128/iai.47.1.329-331.1985.
The administration of sublethal doses of Escherichia coli O111:B4 endotoxin to starved rats results in significant increases in plasma ammonia, free fatty acids, and serum lactate compared with starved controls. These metabolic alterations are associated with Reye syndrome-like histological findings of hepatic microvesicular fatty accumulation and hepatic ultrastructural evidence of mitochondrial pleomorphism with matrix disruption. This sublethal endotoxin model may help elucidate the relationship between the hepatic mitochondrial injury, characteristic metabolic impairment, and encephalopathy seen in patients with Reye syndrome.
与饥饿对照组相比,给饥饿的大鼠注射亚致死剂量的大肠杆菌O111:B4内毒素会导致血浆氨、游离脂肪酸和血清乳酸显著增加。这些代谢改变与瑞氏综合征样的组织学表现相关,即肝微泡性脂肪蓄积,以及线粒体多形性伴基质破坏的肝脏超微结构证据。这种亚致死性内毒素模型可能有助于阐明瑞氏综合征患者肝脏线粒体损伤、特征性代谢损害和脑病之间的关系。