Lou M, Zhang H, Wang J, Wen S-Q, Tang Z-Q, Chen Y-Z, Yan W-Q, Ding M-P
Department of Neurology, The Second Affiliated Hospital, Zhejiang University, School of Medicine, Hangzhou, 310009, People's Republic of China.
Neuroscience. 2007 May 11;146(2):555-61. doi: 10.1016/j.neuroscience.2007.01.046. Epub 2007 Mar 23.
Cerebral hypoxia may be the main component of cell damage caused by ischemia. Previous studies demonstrated a neuroprotective effect of early hyperbaric oxygen (HBO) treatment in various animal models of focal cerebral ischemia. Neuropathologic study showed that exposure of HBO may prevent cell death in ischemic cortex. In the present study, we aimed to assess cellular function of ischemic rat brain after HBO treatment by means of a high-resolution positron emission tomography scanner (microPET) used specifically for small animal imaging. The male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO), with the regional cerebral blood flow monitored in vivo by laser Doppler flowmetry. One hour after ischemia, HBO therapy (3 atm absolute, 1 h) was initiated. Local cerebral glucose utilization in the ischemic area was measured before, 1 h and 3 h after ischemia, with 2-[(18)F]-fluoro-2-deoxy-d-glucose (FDG) as a tracer. Neurological deficits and infarct volumes were assessed at 24 h after ischemia. Our study showed that early HBO therapy significantly reduced infarct volume of brain 24 h after ischemia. Moreover, glucose utilization in the ischemic area underwent a severe decrease during 1-3 h after MCAO, while the early HBO treatment significantly attenuated the decrease in cerebral metabolic rate of glucose in the ischemic core of the cortex compared with controls. We report for the first time the application of microPET to quantify the rates of glucose metabolism in the ischemic core of rats exposed to HBO. Our results suggest that the early exposure of HBO can partially reverse the downward trend for glucose utilization in the ischemic core, which might contribute to the reported beneficial effects of early HBO therapy on permanent cerebral ischemia.
脑缺氧可能是缺血所致细胞损伤的主要组成部分。先前的研究表明，早期高压氧（HBO）治疗在各种局灶性脑缺血动物模型中具有神经保护作用。神经病理学研究显示，HBO暴露可能预防缺血皮层中的细胞死亡。在本研究中，我们旨在通过专门用于小动物成像的高分辨率正电子发射断层扫描仪（microPET）评估HBO治疗后缺血大鼠脑的细胞功能。雄性Sprague-Dawley大鼠接受永久性大脑中动脉闭塞（MCAO），通过激光多普勒血流仪在体内监测局部脑血流量。缺血1小时后开始HBO治疗（绝对压力3个大气压，1小时）。以2-[(18)F]-氟-2-脱氧-D-葡萄糖（FDG）作为示踪剂，在缺血前、缺血后1小时和3小时测量缺血区域的局部脑葡萄糖利用率。在缺血后24小时评估神经功能缺损和梗死体积。我们的研究表明，早期HBO治疗在缺血后24小时显著减少了脑梗死体积。此外，MCAO后1-3小时缺血区域的葡萄糖利用率严重下降，而与对照组相比，早期HBO治疗显著减轻了皮层缺血核心区脑葡萄糖代谢率的下降。我们首次报道了应用microPET定量测定接受HBO治疗的大鼠缺血核心区的葡萄糖代谢率。我们的结果表明，早期暴露于HBO可部分逆转缺血核心区葡萄糖利用率的下降趋势，这可能有助于解释早期HBO治疗对永久性脑缺血的有益作用。
