Van Nimmen D, Weyne J, Demeester G, Leusen I
Am J Physiol. 1984 Oct;247(4 Pt 2):R639-45. doi: 10.1152/ajpregu.1984.247.4.R639.
Cerebral glucose metabolism (CMRglu) is decreased during acute and prolonged hypercapnic acidosis and during prolonged metabolic (HCl) acidosis; it is increased in acute (hypocapnic) metabolic acidosis and is not changed in acute isocapnic metabolic acidosis. The alteration in CMRglu can be explained by the changes occurring in intracerebral pH under these experimental conditions. In pontine gray matter, n. tractus solitarii, and n. ambiguus, three structures participating in the neuronal regulation of ventilation, local CMRglu is increased in all acidotic groups, suggesting coupling of function and metabolism at the local level during acidosis-induced hyperventilation.
在急性和持续性高碳酸性酸中毒以及持续性代谢性（盐酸）酸中毒期间，脑葡萄糖代谢（CMRglu）降低；在急性（低碳酸性）代谢性酸中毒时升高，而在急性等碳酸性代谢性酸中毒时无变化。CMRglu的改变可由这些实验条件下脑内pH值的变化来解释。在脑桥灰质、孤束核和疑核这三个参与通气神经元调节的结构中，所有酸中毒组的局部CMRglu均升高，提示在酸中毒诱导的过度通气期间局部存在功能与代谢的耦合。
