Miller L P, Villeneuve J B, Oldendorf W H
Neurochem Res. 1986 Apr;11(4):489-95. doi: 10.1007/BF00965318.
The present investigation examined the effects of pretreatment with 3-O-methyl-D-glucose (3OMG) or 2-deoxy-D-glucose (2DOG) on post-mortem rise in rat brain lactate to evaluate their potential use for minimizing ischemia-induced rise in brain lactate. The results showed that iv administration of either glucose analogue (2 g/kg) at 2.5 min prior to sacrifice significantly attenuated (to 0.61 of control levels) post-mortem brain lactate rise. Pretreating rats with 2-deoxy-D-glucose (2 g/kg) 15 min prior to sacrifice resulted in a greater inhibition (to 0.52 of control) of the post-mortem lactate rise. The effects of these two analogues (3OMG and 2DOG) can be accounted for by their inhibition of brain glucose transport and inhibition of brain glucose metabolism by 2DOG. The present results suggest that intervention with either of these glucose analogues under the proper experimental procedures may minimize the cytopathological consequences of ischemia related to the rise in brain lactate.
本研究检测了用3 - O - 甲基 - D - 葡萄糖（3OMG）或2 - 脱氧 - D - 葡萄糖（2DOG）预处理对大鼠脑死后乳酸升高的影响，以评估它们在最小化缺血诱导的脑乳酸升高方面的潜在用途。结果显示，在处死前2.5分钟静脉注射任何一种葡萄糖类似物（2 g/kg）均可显著减轻（降至对照水平的0.61）脑死后乳酸升高。在处死前15分钟用2 - 脱氧 - D - 葡萄糖（2 g/kg）预处理大鼠，对死后乳酸升高的抑制作用更大（降至对照的0.52）。这两种类似物（3OMG和2DOG）的作用可归因于它们对脑葡萄糖转运的抑制以及2DOG对脑葡萄糖代谢的抑制。目前的结果表明，在适当的实验程序下，用这些葡萄糖类似物中的任何一种进行干预，可能会将与脑乳酸升高相关的缺血细胞病理学后果降至最低。
