Pharmacologic adjuncts to protect the spinal cord during transient ischemia

Despite numerous strategies that aim to maintain and restore adequate spinal cord perfusion during thoracoabdominal aortic aneurysm repair, a lower limb neurologic deficit remains a distinct possibility. When critical intercostal arteries originate either at or below the level of repair, transient spinal cord ischemia might occur. Pending on the severity and duration of ischemia, irreversible damage evolves. Therefore, it would be advantageous if adjuncts were available that could enhance neuronal tolerance and improve neuronal survival after episodes of spinal cord ischemia. The beneficial effect of permissive or induced hypothermia is well established. This review focuses on pharmacologic adjuncts. The cascade that leads to neuronal death after ischemia consists of several pathways that act both parallel and sequential. The ischemic cascade provides logical pathogenetic determinants for pharmacologic interventions. Indeed, neuroprotection was attributed to numerous agents in experimental spinal cord ischemia. The clinical use of most of these agents is hampered by their toxicity and side effects. The current status of pharmacologic protection against spinal cord ischemia is summarized, and future directions are provided.