Resistance of isolated mammalian spinal cord white matter to oxygen-glucose deprivation
Resistance of isolated mammalian spinal cord white matter to oxygen-glucose deprivation
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DOI：
10.1152/ajpcell.00591.2001
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发表时间：
2002-09-01
影响因子：
5.5
通讯作者：
Shi, RY
中科院分区：
文献类型：
--
作者：
Peasley, MA;Shi, RY
我们发现离体豚鼠脊髓白色物质对急性缺糖缺氧有抵抗作用。60分钟的氧-葡萄糖剥夺导致复合动作电位（CAP）电导降低60%，60分钟后再灌注几乎完全恢复。相应的辣根过氧化物酶排斥试验显示轴突膜损伤很小。为了进一步剥夺轴突的代谢底物，我们在缺血介质中加入2 mM氰化钠或2 mM叠氮化钠（均为线粒体抑制剂），这完全消除了CAP，并导致再灌注后15至30%的恢复。这两种化合物优先降低大直径轴突的电导。我们认为，在我们的缺血模型中，残留的ATP可以保护缺血损伤后脊髓轴突的解剖完整性和生理功能。这进一步表明，氧-葡萄糖剥夺不能单独负责短期的功能和解剖损伤。体内缺血的损伤作用可能由源自脊髓灰质的因子或其他全身性因子介导;在我们的体外白色物质制备中，这两种因子均被大部分消除。
We found that isolated guinea pig spinal cord white matter is resistant to acute oxygen-glucose deprivation. Sixty minutes of oxygen-glucose deprivation resulted in a 60% reduction of compound action potential (CAP) conductance, and there was a near complete recovery after 60 min reperfusion. Corresponding horseradish peroxidase-exclusion assay showed little axonal membrane damage. To further deprive the axons of metabolic substrate, we added 2 mM sodium cyanide or 2 mM sodium azide, both mitochondrial suppressors, to the ischemic medium, which completely abolished CAP and resulted in a 15 to similar to30% recovery postreperfusion. Both compounds preferentially reduced the conductance of large diameter axons. We suggest the residual ATP in our ischemic model can protect anatomic integrity and physiological functioning of spinal axons following ischemic insult. This further suggests that oxygen-glucose deprivation alone cannot be solely responsible for short-term functional and anatomic damage. The damaging effects of ischemia in vivo may be mediated by factors originating from the gray matter of the cord or other systemic factors; both were largely eliminated in our in vitro white matter preparation.