Boris-Möller F, Drakenberg T, Elmdén K, Forsén S, Siesjö B K
Department of Physical Chemistry II, Lund Institute of Technology, Sweden.
Neurosci Lett. 1988 Feb 15;85(1):113-8. doi: 10.1016/0304-3940(88)90439-9.
Ischemia leads to intracellular acidosis, the severity of which depends on the availability of glucose for production of lactate and H+. It has been suggested that major compartmentalization of H+ occurs, with glial cells becoming much more acidotic than neurons. Since this issue is of crucial importance for the understanding of mechanisms of ischemic brain damage, we induced complete ischemia by decapitation in hypo-, normo- and hyperglycemic awake rats, yielding brain tissue lactate contents varying between 4 and 27 mumol/g. Using phosphorus nuclear magnetic resonance (NMR) we explored whether a splitting of the phosphorus peak occurred as a reflection of compartmentalization. Forebrains were put in NMR tubes and spectra obtained 15 min after decapitation. Since no such splitting was observed, we conclude that major compartmentalization does not occur in ischemia at the degrees of lactic acidosis studied.
缺血会导致细胞内酸中毒,其严重程度取决于用于生成乳酸和氢离子的葡萄糖的可利用性。有人提出,氢离子存在主要的分隔现象,即神经胶质细胞比神经元酸化程度更高。由于这个问题对于理解缺血性脑损伤的机制至关重要,我们通过断头法诱导清醒的低血糖、正常血糖和高血糖大鼠完全缺血,得到的脑组织乳酸含量在4至27微摩尔/克之间变化。我们使用磷核磁共振(NMR)来探究磷峰是否会出现分裂,以此作为分隔现象的反映。将前脑放入NMR管中,并在断头后15分钟获取光谱。由于未观察到这种分裂现象,我们得出结论:在所研究的乳酸酸中毒程度下,缺血时不会发生主要的分隔现象。