南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2009年
8期
1638-1640
,共3页
巩守平%王文涛%钟大林%吕健%吴锋%车金%僧志远%贺西京
鞏守平%王文濤%鐘大林%呂健%吳鋒%車金%僧誌遠%賀西京
공수평%왕문도%종대림%려건%오봉%차금%승지원%하서경
脊髓%缺血再灌注%内皮细胞功能%血小板活化%一氧化氮%a颗粒膜蛋白140
脊髓%缺血再灌註%內皮細胞功能%血小闆活化%一氧化氮%a顆粒膜蛋白140
척수%결혈재관주%내피세포공능%혈소판활화%일양화담%a과립막단백140
spinal cord%ischemia/reperfusion%vascular endothelial function%platelet activation%nitric oxide%granule membrane protein 140
目的 探讨内皮细胞功能和血小板活化状态在脊髓缺血再灌注损伤(SCI/RI)中的意义.方法 采用Zivin法建立家兔SCI/RI模型,动态观察SCI/RI前后血浆一氧化氮(NO)和血小板a颗粒膜蛋白140(GMP140)的变化.结果 NO在I/R组缺血末期显著上升(P<0.01),I/R 2h达到峰值,与sham组比较有显著意义(P<0.01);I/R6h下降但仍有显著差异(P<0.05);GMP-140在sham组无显著变化,在I/R组缺血末期显著升高(P<0.01),I/R2h后逐渐下降到正常水平.结论 血浆NO和GMP140在SCI/RI后显著升高,表明内皮细胞受刺激/损伤和血小板过度活化参与了脊髓I/R损伤与修复病理过程.
目的 探討內皮細胞功能和血小闆活化狀態在脊髓缺血再灌註損傷(SCI/RI)中的意義.方法 採用Zivin法建立傢兔SCI/RI模型,動態觀察SCI/RI前後血漿一氧化氮(NO)和血小闆a顆粒膜蛋白140(GMP140)的變化.結果 NO在I/R組缺血末期顯著上升(P<0.01),I/R 2h達到峰值,與sham組比較有顯著意義(P<0.01);I/R6h下降但仍有顯著差異(P<0.05);GMP-140在sham組無顯著變化,在I/R組缺血末期顯著升高(P<0.01),I/R2h後逐漸下降到正常水平.結論 血漿NO和GMP140在SCI/RI後顯著升高,錶明內皮細胞受刺激/損傷和血小闆過度活化參與瞭脊髓I/R損傷與脩複病理過程.
목적 탐토내피세포공능화혈소판활화상태재척수결혈재관주손상(SCI/RI)중적의의.방법 채용Zivin법건립가토SCI/RI모형,동태관찰SCI/RI전후혈장일양화담(NO)화혈소판a과립막단백140(GMP140)적변화.결과 NO재I/R조결혈말기현저상승(P<0.01),I/R 2h체도봉치,여sham조비교유현저의의(P<0.01);I/R6h하강단잉유현저차이(P<0.05);GMP-140재sham조무현저변화,재I/R조결혈말기현저승고(P<0.01),I/R2h후축점하강도정상수평.결론 혈장NO화GMP140재SCI/RI후현저승고,표명내피세포수자격/손상화혈소판과도활화삼여료척수I/R손상여수복병리과정.
Objective To study the changes of vascular endothelial cell function and platelet activation in rabbit spinal cord following ischemia-reperfusion (I/R) injury and their roles in the spinal cord injury. Methods Rabbit spinal cord I/R injury models were established using Zivin method, and the changes in plasma NO and GMP140 levels were dynamically monitored after the injury. Results Plasma NO level increased significantly in the I/R group at the end of the ischemia, and reached the peak level at 2 h of reperfusion as compared to that in sham-operated group (P<0.01). Plasma NO level decreased at 6 h of reperfusion, but still significantly higher than the level in the sham-operated group (P<0.05). Plasma GMP140 underwent no significant changes in the sham-operated group, but significantly increased in the I/R group at the end of the ischemia,followed by gradual declination to the normal level at 2 h of reperfusion. Conclusion Spinal cord I/R injury causes overexpressions of NO and GMP140, suggesting the involvement of endothelial cell injury and platelet overactivation in the pathological process and repair of spinal cord I/R injury.