Zieve L, Doizaki W M, Derr R F
Gut. 1979 Jan;20(1):28-32. doi: 10.1136/gut.20.1.28.
Ammonia coma was produced in rats within 10 to 15 minutes of an intraperitonealinjection of 1.7 mmol NH4CL. This coma was prevented with 1.68 mmol L-dopa given by gastric intubation 15 minutes before the ammonium salt injection. The effect of L-dopa was correlated with a decrease in blood and brain ammonia, an increase in brain dopamine, and an increase in renal excretion of ammonia and urea. Intraventricular infusion of dopamine sufficient to raise the brain dopamine to the same extent did not prevent the ammonia coma nor affect the blood and brain ammonia concentrations. Bilateral nephrectomy eliminated the beneficial effect of L-dopa on blood and brain ammonia and the ammonia coma was not prevented. Thus, the reduction in blood and brain ammonia and the prevention of ammonia coma after L-dopa, can be accounted for by the peripheral effect of dopamine on renal function rather than its central action. These results provide a reasonable explanation for the beneficial effects observed in some encephalopathic patients receiving L-dopa.
给大鼠腹腔注射1.7 mmol氯化铵后10至15分钟内可引发氨昏迷。在注射铵盐前15分钟经胃管给予1.68 mmol左旋多巴可预防这种昏迷。左旋多巴的作用与血氨和脑氨水平降低、脑多巴胺增加以及氨和尿素肾排泄增加相关。脑室内输注足以使脑多巴胺升高至相同程度的多巴胺并不能预防氨昏迷，也不影响血氨和脑氨浓度。双侧肾切除消除了左旋多巴对血氨和脑氨的有益作用，且不能预防氨昏迷。因此，左旋多巴后血氨和脑氨的降低以及氨昏迷的预防可归因于多巴胺对肾功能的外周作用而非其中心作用。这些结果为一些接受左旋多巴治疗的脑病患者所观察到的有益效果提供了合理的解释。
