Matsuyama Y, Sato K, Kamiya M, Yano J, Iwata H, Isobe K
Department of Orthopaedic Surgery, Nagoya University School of Medicine, Japan.
J Spinal Disord. 1998 Jun;11(3):248-52.
To determine whether nitric oxide (NO) is related to spinal cord cavitation, we treated mice that underwent spinal cord injury with NG-mono-methyl-L-arginine (N-MMA). Spinal cord specimens were subjected to glial fibrillary acidic protein (GFAP) immunostaining, which is selective for astrocytes. Spinal cord cavities and GFAP-positive glial cells appeared simultaneously at 3 days after spinal cord injury, and the cavities enlarged at 7 days. In mice receiving N-MMA, the cavities were significantly smaller than those in the mice that underwent spinal cord injury only. However, the numbers of GFAP-positive cells showed no difference between these two groups. These experimental findings suggest that cavitation of the spinal cord is caused mainly by NO released from activated glial cells.
为了确定一氧化氮(NO)是否与脊髓空洞症有关,我们用N-单甲基-L-精氨酸(N-MMA)处理脊髓损伤的小鼠。脊髓标本进行了胶质纤维酸性蛋白(GFAP)免疫染色,该染色对星形胶质细胞具有选择性。脊髓空洞和GFAP阳性胶质细胞在脊髓损伤后3天同时出现,且空洞在7天时扩大。在接受N-MMA的小鼠中,空洞明显小于仅接受脊髓损伤的小鼠。然而,这两组之间GFAP阳性细胞的数量没有差异。这些实验结果表明,脊髓空洞主要由活化胶质细胞释放的NO引起。