J Pryor1, R Shi. 1. Department of Basic Medical Sciences, Institute for Applied Neurology, Purdue University, West Lafayette, IN 47907, USA.
Abstract
STUDY DESIGN: In vitro studies using isolated guinea pig spinal cord white matter. OBJECTIVES: To determine whether lack of oxygen can cause irreversible impairment of electrical impulse conduction. SETTING: Department of Basic Medical Sciences, Purdue University, West Lafayette, Indiana, USA. METHODS: The hypoxic injury was induced by reducing the oxygen tension of the perfused solution by 80%. Compound action potentials (CAPs) were monitored before, during, and after oxygen deprivation. RESULTS: We have found that 60 min of hypoxia reduced the conduction to 30% of preinjury level and recovered to approximately 60% of the preinjury level upon reoxygenation. Larger axons appeared to be more vulnerable to oxygen deprivation. We noted a significant decrease and recovery of the depolarizing afterpotential (DAP). Likewise, there was a delay and recovery of absolute and relative refractory period. Concomitantly, the ability of axons to follow repetitive stimuli was suppressed following oxygen deprivation but recovered upon reoxygenation. CONCLUSION: Following 60 min of oxygen deprivation and 30 min of reoxygenation, mammalian spinal cord white matter can partially recover electrical impulse conduction. However, within the same period, cords gained a complete recovery of other electrical properties, such as the depression of DAP, the delaying of refractory period, and the decreased ability to respond to repetitive stimuli. Compared to previous findings when both oxygen and glucose were deprived, we conclude that glucose plays a relatively minor role during the acute stage of oxygen deprivation in mammalian spinal cord white matter.
STUDY DESIGN: In vitro studies using isolated guinea pigspinal cord white matter. OBJECTIVES: To determine whether lack of oxygen can cause irreversible impairment of electrical impulse conduction. SETTING: Department of Basic Medical Sciences, Purdue University, West Lafayette, Indiana, USA. METHODS: The hypoxic injury was induced by reducing the oxygen tension of the perfused solution by 80%. Compound action potentials (CAPs) were monitored before, during, and after oxygen deprivation. RESULTS: We have found that 60 min of hypoxia reduced the conduction to 30% of preinjury level and recovered to approximately 60% of the preinjury level upon reoxygenation. Larger axons appeared to be more vulnerable to oxygen deprivation. We noted a significant decrease and recovery of the depolarizing afterpotential (DAP). Likewise, there was a delay and recovery of absolute and relative refractory period. Concomitantly, the ability of axons to follow repetitive stimuli was suppressed following oxygen deprivation but recovered upon reoxygenation. CONCLUSION: Following 60 min of oxygen deprivation and 30 min of reoxygenation, mammalianspinal cord white matter can partially recover electrical impulse conduction. However, within the same period, cords gained a complete recovery of other electrical properties, such as the depression of DAP, the delaying of refractory period, and the decreased ability to respond to repetitive stimuli. Compared to previous findings when both oxygen and glucose were deprived, we conclude that glucose plays a relatively minor role during the acute stage of oxygen deprivation in mammalianspinal cord white matter.
Authors: Jill H Fowler; Jamie McQueen; Philip R Holland; Yasmina Manso; Martina Marangoni; Fiona Scott; Emma Chisholm; Robert H Scannevin; Giles E Hardingham; Karen Horsburgh Journal: J Cereb Blood Flow Metab Date: 2017-06-13 Impact factor: 6.200