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目的与方法 :采用Fura 2 /AM探针技术观察NH4 Cl对离体急性分离之Wistar乳鼠大脑细胞胞浆游离钙[Ca2 +]i 含量的影响。结果 :NH4 +浓度为 2 .5mmol/L时脑细胞内 [Ca2 +]i 含量升高。在一定范围内 ,随着NH4 +浓度的加大 ,细胞内Ca2 +持续升高。NH4 +的升钙作用主要被Nicardipine所阻断 ,其变化特征类以KCl。 结论 :NH4 +主要通过影响电压依赖性钙离子通道的开启而导致细胞内钙稳态失调。氨中毒时所引起的各种脑的功能 ,代谢及结构改变有可能通过细胞内钙稳态失调机制实现
PURPOSE AND METHODS: Fura 2 / AM probe was used to observe the effect of NH4Cl on the content of [Ca2 +] i in cytoplasm of brain cells of Wistar rats isolated acutely. Results: When the concentration of NH4 + was 2.5mmol / L, the content of [Ca2 +] i in brain cells increased. Within a certain range, with the increase of NH4 + concentration, intracellular Ca2 + continuously increased. The up-regulation of NH4 + was mainly blocked by Nicardipine, which was characterized by KCl. CONCLUSIONS: NH4 + causes a disturbance of intracellular calcium homeostasis mainly by affecting the opening of voltage-dependent calcium channels. Ammonia poisoning caused by a variety of brain function, metabolism and structural changes may be achieved through the mechanism of intracellular calcium homeostasis