Postischemic reperfusion of the spinal cord: Prolonged reperfusion alleviates the metabolic alterations induced by 25 min ischemia in the cervical and thoracolumbal segments

In recent years, increasing amount of information has indicated that in som e tissues the main damage due to oxidative stress does not occur during rep erfusion but during the ischemic episode of the ischemia/reperfusion event. In this respect, serious doubts were also expressed about the origin of th e increased amounts of free radicals which were believed to form and report ed to appear in the perfusate during the first minutes of reperfusion. More over, speculative explanations were only available for a second increase in lipid peroxidation which was reported to occur after postischemic reperfus ions exceeding 60 min. For this reasons, the present paper reports the results of investigation of ischemia/reperfusion injury to the cervical (CE) and thoracolumbal (ThL) s egments of the spinal cord (SP) after an acute 25 min occlusion of the abdo minal aorta, followed by 60-120 min reperfusion of the ischemic areas in ra bbits. In CE and ThL segments of the SP, the ischemia induced: 1) a decreas e in activities of superoxide dismutase (SOD), from 57.35 +/- 6.36 to 45.27 +/- 5.45 U.mg(-1).min(-1) (S.E.M., 20.92 %), p < 0.01, and from 58.36 <plu s/minus> 5.45 to 33.00 +/- 4.55 U.mg(-1).min(-1) (S.E.M., 43.46 %), p < 0.0 01; 2) a significant decrease in <gamma>-glutamyl transpeptidase (gamma -GT P), from 114.66 +/- 1.45 to 99.88 +/- 4.4 mu mol p-nitroaniline.mg(-1).h(-1 ) (S.E.M. 12.89 %), p < 0.05 and from 112.24 <plus/minus> 1.20 to 95.09 +/- 2.40 mu mol p-nitroaniline.mg(-1).h(-1) (S.E.M., 16.26 %), p < 0.05; 3) a considerable depression in Na,K-ATPase activity, from 7.14 <plus/minus> 0.5 8 to 5.08 +/- 0.32 mu mol P-i. mg(-1).h(-1) (S.E.M., 28.86 %), p < 0.01, an d from 7.23 <plus/minus> 0.11 to 5.09 +/- 0.31 mu mol P-i. mg(-1).h(-1) (S. E.M., 30.00 %), p < 0.01.