1. Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, Sendai, Japan
2. ^‡Department of Neurology, Tohoku University School of Medicine, Sendai, Japan
3. ^*Department of Physiology, Tokai University School of Medicine, Isehara, Japan
4. ^†Department of Neurology, Tokai University School of Medicine, Isehara, Japan

Correspondence: Masahiro Sakurai, Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-77, Japan.

Received 29 December 1997; Revised 23 February 1998; Accepted 24 February 1998.

Abstract

The induction and distribution of 3-L-nitrotyrosine (NO₂-Tyr) were examined with HPLC and immunohistochemistry in rabbit spinal cords after 15 minutes of transient ischemia until 7 days of the reperfusion. After the 15-minute ischemia, there was a significant decrease of neurologic scores in the ischemic group compared with the sham-operated control group at 7 days of reperfusion (P = 0.0017), and the majority of motor neurons was selectively lost at 7 days of reperfusion (P = 0.0039). NO₂-Tyr was transiently induced at 8 hours of reperfusion in the ventral part of the spinal cord (0.47% 0.86%, NO₂-Tyr/total tyrosine; P = 0.0021), but was not induced at any time point of reperfusion in the dorsal part of the spinal cord. Strong immunoreactivity for NO₂-Tyr was selectively induced in large pyramidal motor neurons at 8 hours of reperfusion and was still weakly present until 7 days of reperfusion. (There may be a difference in sensitivity between the two techniques.) These results suggested that protein tyrosine nitration by nitric oxide plays a role in the selective motor neuron cell damage after transient spinal cord ischemia.