Ischemic tolerance after spinal cord ischemia

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We investigated the effect of interval between brief spinal cord ischemia and subsequent severe ischemic insult on hindlimb motor function and histopathology of the spinal cord. To explore the mechanism of spinal ischemic tolerance, induction of 70- kDa heat shock protein (HSP70) was also evaluated.A brief spinal cord ischemia was produced by occlusion of the abdominal aorta during isoflurane anesthesia. Recirculation after brief ischemia was started when the third negative wave of segmental spinal cord evoked potential disappeared. This ischemic insult did not produce neuronal damage in the spinal cord. Two days, 4 days, or 7 days (n=8 in each) following the first ischemia, the animals (double ischemia group) were subjected to the second ischemia for 20 minutes. The single ischemia group received a sham procedure instead of the first ischemia and was identically subjected to the second ischemia 4 days following the sham procedure. Two days following the second ischemia, hindlimb motor function was evaluated. After perfusion and fixation of the spinal cord, normal neurons in the anterior lumber spinal cord were counted.The neurologic status and histopathology in the animals in the double ischemia group subjected to the second ischemia 4 days after first ischemia were significantly better than in the single ischemia group. HSP70 was induced 2 days, 4 days, and 7 days after brief spinal cord ischemia. Intense HSP70 staining was observed 4 hours after second ischemic insult in all animals that showed normal neurologic function regardless of preconditioning with brief spinal cord ischemia.These results suggest that ischemic tolerance was observed 4 days, but not adequately 2 or 7 days after brief spinal cord ischemia and that factors other than HSP70 may play an important role in the mechanism of spinal ischemic tolerance.