Hukuda S, Mochizuki T, Ogata M
Neurosurgery. 1980 Jun;6(6):639-43. doi: 10.1227/00006123-198006000-00004.
Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
在急性脊髓损伤后24小时，通过极谱法在脊髓背侧测量脊髓组织氧，并研究高血压、高碳酸血症和高氧的影响。用充气至400毫米汞柱的硬膜外止血带压迫杂种犬胸段脊髓中部造成急性脊髓损伤，持续5分钟。在损伤部位，脊髓组织氧在损伤后立即略有增加，但在1小时时显著降低，此后保持不变。静脉输注去甲肾上腺素引起的高血压在3小时后仅使组织氧略有升高。用95%氧气:5%二氧化碳混合气体通气产生的高碳酸血症和高氧并未提高降低的脊髓氧含量。当高血压、高碳酸血症和高氧联合使用时，即使在损伤后3小时脊髓氧处于最低水平时，脊髓氧值也升高到正常水平，此后稳步增加。
