Nagai Y, Naruse S, Weiner M W
Department of Medicine, Veterans Administration Medical Center, San Francisco, California 94121.
NMR Biomed. 1993 Jan-Feb;6(1):1-6. doi: 10.1002/nbm.1940060102.
Previous investigators have attributed the fall of brain intracellular pH (pHi) produced by ischemia to accumulation of lactic acid. The goal of the present experiments was to examine the hypothesis that the acidosis produced by cerebral ischemia is due to accumulation of lactic acid. The present experiments inhibited lactic acid production by lowering glucose availability using insulin-induced hypoglycemia. The adverse effects of hypoglycemia were prevented by the prior elevation of beta-hydroxybutyric acid and acetoacetic acid induced by a high lipid diet. Brain pHi and lactic acid were measured by 31P and 1H NMR. The results showed that insulin-induced hypoglycemia markedly inhibits production of lactic acid, but has no effect on brain pHi during ischemia. These findings suggest that, at least under some conditions, the acidosis produced by cerebral ischemia is not due to accumulation of lactic acid.
先前的研究人员将缺血导致的脑细胞内pH值(pHi)下降归因于乳酸的积累。本实验的目的是检验以下假设:脑缺血产生的酸中毒是由于乳酸积累所致。本实验通过胰岛素诱导的低血糖降低葡萄糖供应来抑制乳酸生成。高脂饮食诱导的β-羟基丁酸和乙酰乙酸预先升高可预防低血糖的不良反应。通过31P和1H核磁共振测量脑pHi和乳酸。结果表明,胰岛素诱导的低血糖显著抑制乳酸生成,但在缺血期间对脑pHi没有影响。这些发现表明,至少在某些情况下,脑缺血产生的酸中毒并非由于乳酸积累。