Roberts E L, He J, Chih C P
Geriatric Research, Education, and Clinical Center, Miami VA Medical Center, Miami, FL 33125, USA.
Brain Res. 2000 Sep 1;875(1-2):171-4. doi: 10.1016/s0006-8993(00)02587-7.
The purpose of this study was to see how the nominal removal of bicarbonate (HCO(-)(3)) from the extracellular space of brain tissue influenced recovery of brain tissue from anoxia. Removal of HCO(-)(3) in HEPES-buffered artificial cerebrospinal fluid (aCSF) inhibited almost completely recovery of synaptic transmission in hippocampal slices after anoxia. Altered pH did not contribute to this finding because adjusting intracellular (pH(i)) and extracellular (pH(o)) pH to control levels did not reduce the effect of HCO(-)(3) removal. Our results suggest that HCO(-)(3) levels are important in determining the extent of anoxic or ischemic brain injury.
本研究的目的是观察从脑组织细胞外空间名义上去除碳酸氢根（HCO₃⁻）如何影响脑组织从缺氧状态的恢复。在HEPES缓冲的人工脑脊液（aCSF）中去除HCO₃⁻几乎完全抑制了缺氧后海马切片中突触传递的恢复。pH的改变对此结果无影响，因为将细胞内（pH(i)）和细胞外（pH(o)）pH调节至对照水平并不能降低去除HCO₃⁻的作用。我们的结果表明，HCO₃⁻水平在确定缺氧或缺血性脑损伤的程度中很重要。
