Nishibe M
Second Department of Surgery, Hokkaido University School of Medicine, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1989 May;64(3):301-8.
I have developed the new procedure for the preparation of experimental ischemic spinal cord from dog. Using this preparation, I have measured the enzymatic activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase. The ischemic spinal cords, monitored by the evoked spinal cord potential, were obtained after clamping bilateral subclavian arteries and aorta distal to the origin of the left subclavian artery. Total SOD activity of the normal spinal cord was one ninth lower than that of the brain. But its catalase activity was eight times higher. Total SOD, Mn-SOD, and glutathione peroxidase activities of my experimental ischemic spinal cord didn't change as compared with those of the normal ones. The catalase activity was decreased after spinal cord ischemia. These results indicate that the catalase plays the main of protection against peroxidative damage in the spinal cord induced by reperfusion, Ca++-dependent protease system may be involved in the decrease for catalase activity in addition to the high turnover rate of this enzyme. In summary, ischemic injury of spinal cord could be induced from the active oxygen species as well as disorder of Ca++ in the tissue.
我已经开发出了一种用于制备犬实验性缺血性脊髓的新方法。利用这种制备方法,我测量了超氧化物歧化酶(SOD)、过氧化氢酶和谷胱甘肽过氧化物酶的酶活性。通过脊髓诱发电位监测,在钳夹双侧锁骨下动脉和左锁骨下动脉起始部远端的主动脉后,获得缺血性脊髓。正常脊髓的总SOD活性比脑低九分之一。但其过氧化氢酶活性高八倍。与正常脊髓相比,我的实验性缺血性脊髓的总SOD、锰超氧化物歧化酶和谷胱甘肽过氧化物酶活性没有变化。脊髓缺血后过氧化氢酶活性降低。这些结果表明,过氧化氢酶在对抗再灌注诱导的脊髓过氧化损伤中起主要保护作用,除了该酶的高周转率外,钙依赖蛋白酶系统可能参与了过氧化氢酶活性的降低。总之,脊髓缺血性损伤可能由活性氧物质以及组织中钙紊乱引起。