Siemkowicz E
Acta Neurol Scand. 1981 Sep;64(3):207-16. doi: 10.1111/j.1600-0404.1981.tb04400.x.
Glucose treatment prior to cerebral ischemia is followed by similar metabolic and hemodynamic recovery (Siemkowicz & Gjedde 1980), and normalisation of brain extracellular ions (Siemkowicz & Hansen 1981). In view of this, the present study investigated whether post-ischemic hyperglycemia influenced recovery from cerebral ischemia. In rats which received 50% glucose during a 10 min period of cerebral ischemia, and which had a plasma glucose level of 28.5 mM after 10 min of recirculation, recovery was inferior to that of rats receiving either 8% NaCl or 0.9% NaCl (and hence the rats were normoglycemic). Furthermore, rats which had been rendered hyperglycemic (39 mM) prior to ischemia, and which had plasma glucose lowered to 15 mM by insulin treatment during ischemia, did not recover and died within 4 days. Conversely, rats with somewhat lower preischemic hyperglycemia (28 mM), and which had plasma glucose lowered to 12 mM by insulin treatment during ischemia, recovered as well as the normoglycemic rats. In conclusion, preischemic and postischemic hyperglycemia is detrimental to recovery from cerebral ischemia.
脑缺血前进行葡萄糖治疗后会出现类似的代谢和血流动力学恢复（Siemkowicz和Gjedde，1980年），以及脑细胞外离子的正常化（Siemkowicz和Hansen，1981年）。鉴于此，本研究调查了缺血后高血糖是否会影响脑缺血的恢复。在脑缺血10分钟期间接受50%葡萄糖的大鼠中，再灌注10分钟后血浆葡萄糖水平为28.5 mM，其恢复情况比接受8%氯化钠或0.9%氯化钠（因此这些大鼠血糖正常）的大鼠要差。此外，在缺血前血糖已升高至39 mM的大鼠，在缺血期间通过胰岛素治疗使血浆葡萄糖降至15 mM，这些大鼠没有恢复并在4天内死亡。相反，缺血前高血糖程度稍低（28 mM）且在缺血期间通过胰岛素治疗使血浆葡萄糖降至12 mM的大鼠，其恢复情况与血糖正常的大鼠一样。总之，缺血前和缺血后高血糖对脑缺血的恢复是有害的。
