Abstract
1. Motoneurons in the spinal cord are especially vulnerable to ischemic injury and selectively destroyed after transient ischemia. To evaluate the role of nitric oxide (NO) in the pathophysiology of the spinal cord ischemia, the expression of neuronal nitric oxide synthase (nNOS) in the motoneurons of the lumbosacral spinal cord was examined in the rabbit model of transient abdominal aorta occlusion. 2. The aim of the present study was to find if there is any consensus between the duration of transient abdominal aorta occlusion, nNOS positivity of the motoneurons and neurological hind limb impairment. 3. According to the degree of neurological damage (i.e., from the group with almost no sign of damage to a group with fully developed paraplegia), the experimental animals were divided into three groups. The respective spinal cord segments of each experimental group were compared to the control group. 4. Spinal cord ischemia (15 min) was induced by Fogarty arterial embolectomy catheter occlusion of abdominal aorta with a reperfusion period of 7 days. On seventh day, the sections of lumbosacral segments were immunohistochemically treated and L1-L7, and S1-S2 segment sections were monitored using light microscopy.