Inductions of 3-L-nitrotyrosine in motor neurons after transient spinal cord ischemia in rabbits

被引:20
作者
Sakurai, M
Fukuyama, N
Takizawa, S
Abe, K
Hayashi, T
Shinohara, Y
Nakazawa, H
Tabayashi, K
机构
[1] Tohoku Univ, Sch Med, Dept Thorac & Cardiovasc Surg, Aoba Ku, Sendai, Miyagi 98077, Japan
[2] Tohoku Univ, Sch Med, Dept Neurol, Aoba Ku, Sendai, Miyagi 98077, Japan
[3] Tokai Univ, Sch Med, Dept Physiol, Isehara, Kanagawa 25911, Japan
[4] Tokai Univ, Sch Med, Dept Neurol, Isehara, Kanagawa 25911, Japan
关键词
rabbit; spinal cord ischemia; 3-L-nitrotyrosine;
D O I
10.1097/00004647-199811000-00009
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:1233 / 1238
页数:6
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