In the milieu of the postischemic nerve system, oxygen plays an important, but different role on the ischemia/reperfusion injury. Oxygen is needed in newly restored oxidative phosphorylation to reenergize neurons depleted of ATP and membrane potential. Alternatively, oxygen may also be used as substrate for the destructive free radical-mediated processes that seem to be common final pathways in numerous mechanisms of ischemia/reperfusion injury. Several investigators have reported decreasing inspired oxygen concentration was neuroprotective. But, others have demonstrated hyperbaric oxygen was useful for reducing the ischemia/reperfusion injury. Our study aims first to evaluate the effects of difference in arterial oxygen tension on early phase of ischemia/reperfusion injury and to outline practical use of oxygen to reduce ischemic/reperfusion injury.

A rabbit spinal cord ischemia model of infrarenal aortic occlusion for 17 mins was employed. Rabbits were randomly assigned to three groups. The rabbits in control group (n = 3) did not undergo ischemic insult. The rabbits in group A (n = 5) and B (n = 5) underwent ischemic insult for 17 mins and then breathed oxygen (6 L/min) via facial mask or room air, respectively. We observed neurologic function for 2 days. The sections of the spinal cords were stained with hematoxylin and eosin, and the number of spinal motor neurons in ventral region was counted by light microscopy.

All rabbits in control group did not have neurologic dysfunction whereas all rabbits in group A and B had neurologic dysfunction at same degree. Spinal motor neurons in ventral gray matter in group A and B decreased significantly compared with those in control group (P < 0.05). But, difference in number between group A and B was not significant.

The result indicated that the level of arterial oxygen tension within the clinical range had little effect on early phase of ischemia/reperfusion injury.