Baran H, Lassmann H, Sperk G, Seitelberger F, Hornykiewicz O
Neuroscience. 1987 Jun;21(3):679-84. doi: 10.1016/0306-4522(87)90029-7.
The effect of mannitol treatment on the behavioural, morphological and neurochemical brain damage induced after subcutaneously applied kainic acid (10 mg/kg) was studied in the rat. Mannitol at a dose of 1.5 g/kg was injected intravenously 10 min, 1.5 h and 3 h respectively after kainic acid administration. A protective effect of mannitol was observed only when mannitol was given 1.5 h after kainic acid application, i.e. within the early phase of kainic acid-induced brain oedema development. At this time period, mannitol prevented the development of kainic acid-induced seizures as well as irreversible brain lesions and neurochemical changes, the latter being reduction of noradrenaline levels in amygdala/pyriform cortex measured 3 h, and reduction of glutamate decarboxylase and choline acetyltransferase activities measured 3 days after kainic acid treatment. Similarly loss of glutamate decarboxylase activity in dorsal hippocampus induced by kainic acid was prevented by mannitol treatment. It is concluded that by washing out brain oedema, mannitol treatment may prevent propagation of seizures and brain damage in the kainic acid model of epilepsy.
研究了甘露醇治疗对皮下注射海藻酸(10mg/kg)诱导的大鼠行为、形态学和神经化学脑损伤的影响。在海藻酸给药后10分钟、1.5小时和3小时分别静脉注射剂量为1.5g/kg的甘露醇。仅当在海藻酸给药后1.5小时给予甘露醇时,即海藻酸诱导的脑水肿发展的早期阶段,观察到甘露醇具有保护作用。在此时间段,甘露醇可预防海藻酸诱导的癫痫发作以及不可逆的脑损伤和神经化学变化,后者包括在3小时时杏仁核/梨状皮质中去甲肾上腺素水平的降低,以及在海藻酸治疗3天后谷氨酸脱羧酶和胆碱乙酰转移酶活性的降低。同样,甘露醇治疗可预防海藻酸诱导的背侧海马谷氨酸脱羧酶活性丧失。得出的结论是,通过消除脑水肿,甘露醇治疗可能预防癫痫发作的传播和癫痫海藻酸模型中的脑损伤。