Since several clinical data have suggested that the incidence of neurological deficit after aortic surgery has not changed appreciably over the last 50 years, anesthesiologists as well as vascular surgeons have attempted to resolve this clinically important issue by employing various strategies to prevent ischemic spinal cord injury. With respect to inhalational anesthetics, it is thought that isoflurane as well as sevoflurane preconditioning might provide neuroprotective effects against spinal ischemia via activation of TWIK-related K channels-1 or the potassium ATP channel. Glutamate receptor antagonists, including ketamine, could also potentially provide some neuroprotection against spinal ischemia. However, it seems likely that decreased glutamate release could produce more neuroprotective effects against spinal ischemia than a blockade of the glutamate receptor. Although barbiturate alone failed to protect the spinal cord, a controversial issue has been the possible neuroprotective effects associated with local anesthetics including tetracaine, lidocaine and bupivacaine. Clinical cases and experimental studies have indicated that neuraxial opioids might be capable of exacerbating neurological deficits even after a non-injurious interval of spinal ischemia. Inhaled nitric oxide (iNO) therapy (40-80ppm), a common treatment for pulmonary hypertension, has been reported to prevent ischemic brain injury in animal studies by selective dilation of collateral arterioles. The vasodilating effects of iNO on the central nervous system might enhance the “collateral network” in the spinal cord during aortic cross-clamp, potentially protecting the spinal cord. In conclusion, some anesthetics, especially inhalational anesthetics, may provide neuroprotective effects against spinal cord ischemia, but administration of neuraxial opioid after spinal cord ischemia might exacerbate neurological dysfunction.