Kobrine A I, Evans D E, Rizzoli H V
Neurosurgery. 1980 Oct;7(4):369-75. doi: 10.1227/00006123-198010000-00010.
In this experiment, the vulnerability of long tract neural conduction in the spinal cord to progressive hypoxia was studied. The physiological integrity of nonsynaptic spinal cord conduction was monitored with the spinal evoked response (SER). Focal spinal cord blood flow was measured with the hydrogen clearance method. Progressive hypoxia was created by progressively increasing the amount of nitrogen in the inspired gas mixture. The SER was seen to fail only after extended periods of severe hypoxia. Multisynaptic cerebral condition monitored by the cerebral evoked response (CER) seemed more sensitive in the three animals in which both SER and CER were recorded. Spinal cord blood flow (SCBF) was not affected by progressive hypoxia until the PO2 was below 40 torr, and then the SCBF rose dramatically with further progression of the hypoxia.
在本实验中，研究了脊髓长束神经传导对进行性缺氧的易损性。采用脊髓诱发电位（SER）监测非突触性脊髓传导的生理完整性。用氢清除法测量脊髓局部血流量。通过逐渐增加吸入气体混合物中的氮气量来制造进行性缺氧。SER仅在长时间严重缺氧后才消失。在记录了SER和大脑诱发电位（CER）的三只动物中，通过CER监测的多突触大脑状况似乎更敏感。脊髓血流量（SCBF）在动脉血氧分压低于40托之前不受进行性缺氧的影响，然后随着缺氧的进一步发展，SCBF急剧上升。
