Background. Spinal cord ischemia (SCI) leads to variable degrees of neurological deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia reperfusion injury is still limited. Since isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to investigate the effect of isoflurane on the spinal cord’s functional recovery in a rat model of cord ischemia.
Methods: Rats were randomly anesthetized by parenteral anesthetic (Zoletil) and isoflurane (0 and 1.5 % v/v in oxygen). Cord ischemia was induced by cross-clamping of thoracic aorta at the level of T5, and cord perfusion was resumed after 25 min. The motor function was assessed independently up to 48 h after reperfusion. Spinal cords were harvested and analyzed for molecular and histological changes.
Results: The locomotor rating scale was significantly reduced in rats that received isoflurane treatment during SCI at 12 to 48 h after reperfusion. Isoflurane enhanced the expression of heme oxygenase-1 and suppressed tissue levels of IL-6. However, the protein expressions of glial fibrillary acidic protein (GFAP), cleaved caspase-3 and Iba-1 were enhanced in the injured spinal cord. Increased apoptotic cells and presence of axonal damage were also observed in the histological sections.
Conclusion: Our results demonstrate that administration of inhaled isoflurane in spinal cord ischemia reperfusion injury deteriorates the recovery of motor function. The neurotoxicity response is associated with neuronal apoptosis and degeneration. This study highlights the potential adverse effect of isoflurane on the functional recovery of ischemic spinal cord during major aortic surgery.

Isoflurane impairs motor function recovery by increasing neuroapoptosis and degeneration during spinal ischemia-reperfusion injury