Krolicki L, Leniger-Follert E
Pflugers Arch. 1980 Sep;387(2):121-6. doi: 10.1007/BF00584262.
Oxygen supply of the brain cortex together with changes in the electrocorticogram (ECoG) were investigated during and after insulin induced hypoglycemia in 13 anaesthetized rats. Local oxygen partial pressures (pO2) on the parietal cortex were continuously measured with a multiwire surface electrode of the Clark type. During early hypoglycemia with a mean arterial glucose concentration [G]a of 2.81 (SD +/- 0.40) mmol/l, the local tissue pO2 did not change significantly as compared to the pO2 values recorded during the control period with a normal [G]a of 4.51 (SD +/- 0.70) mmol/l. During severe hypoglycemia at a [G]a of 1.39 (SD +/- 0.2) mmol/l, pO2 began to increase continuously on all 104 measuring sites, independently of changes in arterial blood pressure and ECoG. During a period of 7-18 min of isoelectricity, tissue pO2 remained elevated so long as blood pressure did not decrease. After injection of a 25% glucose solution, pO2 gradually decreased to control values within 30-60 min in most experiments. We conclude from these results that oxygen supply is generally improved during severe hypoglycemia. We assume that the increase in tissue pO2 is mainly caused by an increase in microflow. Thus, the neuronal damage occurring after severe hypoglycemia, as reported in literature, cannot primarily be caused by an oxygen deficiency.
在13只麻醉大鼠胰岛素诱导的低血糖期间及之后，研究了大脑皮质的氧供应以及脑电图（ECoG）的变化。使用Clark型多线表面电极连续测量顶叶皮质的局部氧分压（pO2）。在平均动脉血糖浓度[G]a为2.81（标准差±0.40）mmol/l的早期低血糖期间，与正常[G]a为4.51（标准差±0.70）mmol/l的对照期记录的pO2值相比，局部组织pO2没有显著变化。在[G]a为1.39（标准差±0.2）mmol/l的严重低血糖期间，所有104个测量部位的pO2开始持续升高，与动脉血压和ECoG的变化无关。在等电位7 - 18分钟期间，只要血压不下降，组织pO2就保持升高。在大多数实验中，注射25%葡萄糖溶液后，pO2在30 - 60分钟内逐渐降至对照值。从这些结果我们得出结论，在严重低血糖期间氧供应通常会改善。我们假设组织pO2的增加主要是由微流量增加引起的。因此，文献报道的严重低血糖后发生的神经元损伤不能主要由缺氧引起。
