WARREN K S, SCHENKER S
Gut. 1963 Mar;4(1):20-6. doi: 10.1136/gut.4.1.20.
The relation between ammonia intoxication and liver disease is not clear. Ammonia appears to be relatively non-toxic to normal individuals, whereas some patients with liver disease appear to be exquisitely sensitive to dietary protein, ammonia-releasing substances, and ammonium salts. In an attempt to elucidate this relationship the intravenous LD(50) of ammonium chloride was determined in both normal mice and in those with liver disease produced by a variety of means. Parenchymal damage was created by acute and chronic carbon tetrachloride intoxication, a low-protein, lipotrope-deficient diet, and mouse hepatitis virus. Mice in which the portal vein had been partially ligated and those infected with Schistosoma mansoni developed portal-systemic collateral circulation. Groups of these mice were placed on high-protein diets and ammonia drinking water for periods as long as two months. A combination of both parenchymal damage and collateral circulation was induced in mice either by bile duct ligation or by a combination of schistosomiasis and acute carbon tetrachloride intoxication. When the above groups of mice with liver disease were compared with normal control mice in the same weight range, the LD(50) of ammonium chloride showed no striking change.
氨中毒与肝脏疾病之间的关系尚不清楚。氨对正常个体似乎相对无毒，而一些肝病患者似乎对膳食蛋白质、氨释放物质和铵盐极为敏感。为了阐明这种关系，测定了正常小鼠以及通过多种方式诱发肝病的小鼠静脉注射氯化铵的半数致死量（LD50）。通过急性和慢性四氯化碳中毒、低蛋白、缺乏促脂物质的饮食以及小鼠肝炎病毒造成实质损伤。门静脉部分结扎的小鼠以及感染曼氏血吸虫的小鼠形成了门体侧支循环。将这些小鼠分组，给予高蛋白饮食并饮用含氨的水，持续长达两个月。通过胆管结扎或血吸虫病与急性四氯化碳中毒相结合的方式，在小鼠中诱导实质损伤和侧支循环同时出现。当将上述患有肝病的小鼠组与相同体重范围的正常对照小鼠进行比较时，氯化铵的LD50没有显著变化。
