Weyne J, Van Leuven F, Kazemi H, Leusen I
J Appl Physiol Respir Environ Exerc Physiol. 1978 Mar;44(3):333-9. doi: 10.1152/jappl.1978.44.3.333.
Glutamic, aspartic, and gamma-aminobutyric acid (GABA), glutamine, and ammonium were measured in the brains of unanesthetized normocapnic and hypercapnic (10% CO2; 5 min to 3 wk) rats. Hypercapnia increased glutamine and GABA and decreased glutamic and aspartic acids. Changes occurred within 1 h and were maintained during the observation period of 3 wk. On return to normocapnia amino acid concentrations were almost normal after 1 h. Based on the time course it is concluded that intracerebral hypercapnia is more likely the stimulus for change than acidosis. Ammonium content was unchanged for at least 1 h after the onset of hypercapnia but increased thereafter. Experiments in which glutamine synthesis by brain was impeded by inhibiting the enzyme glutamine synthetase favor the hypothesis that the rise of ammonium content in hypercapnia is initially not seen because of increased glutamine synthesis. The changes observed may have a role in metabolic pH homeostasis of brain tissue and may also be relevant to the modified brain excitability in hypercapnia.
在未麻醉的正常碳酸血症和高碳酸血症（10%二氧化碳；5分钟至3周）大鼠的大脑中测量了谷氨酸、天冬氨酸、γ-氨基丁酸（GABA）、谷氨酰胺和铵。高碳酸血症会增加谷氨酰胺和GABA，降低谷氨酸和天冬氨酸。这些变化在1小时内出现，并在3周的观察期内持续存在。恢复正常碳酸血症后1小时，氨基酸浓度几乎恢复正常。根据时间进程得出结论，脑内高碳酸血症比酸中毒更有可能是变化的刺激因素。高碳酸血症开始后至少1小时铵含量不变，但此后增加。通过抑制谷氨酰胺合成酶来阻碍大脑谷氨酰胺合成的实验支持了这样一种假设，即高碳酸血症中铵含量最初未见升高是由于谷氨酰胺合成增加。观察到的这些变化可能在脑组织的代谢pH稳态中起作用，也可能与高碳酸血症中大脑兴奋性的改变有关。
