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目的：观察外源性内毒素诱发肝硬化大鼠发生肝性脑病的可能性及可能机制。方法：采用腹腔内小剂量内毒素一次性注射（３００μｇ／１０ｇＢＷ）诱发肝硬化大鼠发生肝性脑病。结果：小剂量内毒素腹腔内注射可以诱发肝硬化大鼠发生肝性脑病。内毒素注射后，动物一般行为状态及脑电图皆有明显变化，与其他肝性脑病模型或肝性脑病病人类似。同时，血氨和胰高血糖素水平显著升高。血浆内毒素含量与血氨、血胰高血糖素含量之间及血氨与血及脑匀浆谷氨酰胺含量之间皆存在明显的正相关。结论：内毒素血症可通过其本身的直接作用或通过胰高血糖素血症导致血氨水平的增高。高氨血症时，氨很可能通过其在脑内的代谢产物－谷氨酰胺而最终影响中枢神经系统的功能、导致脑病的发生。高氨血症是内毒素诱发肝性脑病发生的主要环节之一。
Objective: To observe the possibility and possible mechanism of hepatic encephalopathy induced by exogenous endotoxin in cirrhotic rats. Methods: Hepatic encephalopathy was induced in rats with cirrhosis by intraperitoneal injection of a small dose of endotoxin (300μg / 10gBW). Results: Small doses of endotoxin intraperitoneal injection can induce hepatic encephalopathy in cirrhotic rats. Endotoxin injection, the general state of behavior and EEG animals have significant changes, and other hepatic encephalopathy model or hepatic encephalopathy patients. At the same time, blood ammonia and glucagon levels were significantly elevated. Plasma endotoxin content and blood ammonia, blood glucagon levels and blood ammonia and blood and brain homogenates glutamine content between there is a clear positive correlation. CONCLUSIONS: Endotoxemia can result in an increase in blood ammonia levels either through its own direct action or through glucagon. Ammonia, ammonia is likely through its brain metabolites - glutamine and ultimately affect the central nervous system function, leading to encephalopathy. Hypernatremia is one of the main aspects of endotoxin-induced hepatic encephalopathy.