Abstract
Spinal cord ischemia is one of the most serious complications of aortic repair in patients with acute aortic syndrome. However, the effect of hypotension before aortic clamping on spinal cord injury has not been documented. A total of 48 male Sprague-Dawley rats were randomly divided into four groups: the sham group; control group (mean arterial pressure (MAP) < 90% of baseline value before aortic clamping); mild hypotension group (MAP < 80%); and profound hypotension group (MAP < 60%). Spinal cord ischemia was induced using a balloon-tipped catheter placed in the descending thoracic aorta. Neurological function of the hind limbs was evaluated for seven days after reperfusion and recorded using a motor deficit index (MDI). The spinal cord was then harvested for histopathological examination and evaluation of oxidative stress and inflammation. The profound hypotension group demonstrated a significantly higher MDI 48 h post-reperfusion and lower number of normal motor neurons than the other groups (p < 0.001). The levels of tissue malondialdehyde and tumor necrosis factor-α (TNF-α) were also significantly increased in the profound hypotension group compared with other groups. Profound hypotension before aortic clamping can aggravate neurologic outcomes after aortic surgery by exacerbating neurologic injury and reducing the number of normal motor neurons.