脑组织内pH对于细胞存活具有重要影响，正常生理范围内的pH对于脑内蛋白质的结构及酶作用的发挥尤为重要。缺氧缺血（Hypoxic ischemia, HI）后能量衰竭，细胞膜不能维持离子泵功能，能量衰竭导致去离子化，引起不同的离子通道开放，导致H+在细胞内外分布的变化。电压门控质子通道（Hv1）具有调节细胞内pH的功能。Hv1可以被细胞内酸化环境激活，主要介导外向的H+流，它对质子具有高度选择性而使其他阳离子不能通过该通道。本研究利用新生猪缺氧缺血性脑损伤模型测量缺氧缺血后不同时间点内动脉血中Na+、K+、Ca2+、Lac、pH的变化，结合磁共振波谱成像采集的乳酸、酰胺质子转移APT、组织学测量的Hv1、Na+-K+-ATP酶、Ca2+/CaMPKⅡ结果进行多变量分析，进一步明确HI后脑内H+在神经网络内的穿梭机制。

The pH of brain tissue has important influence on cell survival, and the pH within normal physiological range is particularly important for the structure and enzyme function of brain proteins. After HI, energy failure, cell membrane cannot maintain ion pump function, and energy failure leads to deionization, which leads to the opening of different ion channels, resulting in the change of H+ inside and outside the cell..Voltage-gated proton channel (Hv1) has the function of regulating intracellular pH. Hv1 can be activated by intracellular acidification environment, mainly mediated by the outgoing H+ flow, which is highly selective to the proton and makes other cations cannot pass through the channel..This study using piglet hypoxic ischemic brain damage models to measure different time points after hypoxia ischemia artery of Na+, K+, Ca2+, the change of the lactate, pH, combined with 1H-MRS acquisition of Lac, amide proton transfer imaging, histological measurements Hv1, Na+-K+-ATPase, Ca2+ / CaMPK Ⅱ results multivariate analysis, studies the pH adjustment mechanism after HI, further defined the shuttle mechanism of H+ in the neural network.