摘要
目的通过检测大鼠急性脊髓损伤(Spinalcordinjury,SCI)后伤段脊髓组织内皮素-1(Endothelin-1,ET-1)含量和Ca2+含量的变化,探讨ET-1和Ca2+在继发性脊髓损伤中的作用机制。方法SD雄性大鼠80只,用改良Allen’s打击法,致伤力为50g/cm,造成C6～7段脊髓中度损伤模型后,用放射免疫法和原子吸收光谱分析法测定SCI后2、4、8、24、72h、1周和2周脊髓组织中ET-1和Ca2+的含量。结果损伤节段脊髓组织ET-1和Ca2+含量均随病程而改变,伤后4h达最高峰,并分别持续至48h和72h,于1～2周仍维持较高水平,与正常值有显著性差异。结论SCI后早期伤段脊髓内ET-1和Ca2+含量增高,参与了脊髓继发性损伤,为临床上ET-1受体拮抗剂与Ca2+拮抗剂联合使用来减轻SCI后继发性损伤提供理论依据。
Objective:To study the changes of endothelin 1(ET-1) and intracellular calcium concentration in the injured spinal tissues after acute spinal cord injury(SCI),and disscuss their possible mechanism in secondary SCI. Method:Eighty rats of experimental acute SCI models were created by modified Allen's method with a force of 50 g.cm which caused moderate injury of C6,7.At 2h,4h,8h,24h,72h、lwk and 2wk after injury,changes of ET-1were measured by means of radio-immunoassay,and the intracellular calcium of injured spinal cord were examined by the technique of atomic absorption spectectomy with La3+ blockage.Result:The ET-1 and intracellular calcium level of the involved spinal cord increased significantly with the development of injury and reached their climax at 4h,continued at high level within lwk-2wk after SCI.There was significant difference between the injured team and the normal one.Conclusion:The ET-1 and intracellular calcium,increased in the early stage of SCI are the most important mechanisms associated with secondary injury, and influences each other. The combined appliance of ET-1 receptor inhibitorand calcium channel inhibitor will alleviate secondary SCI.
出处
《中国矫形外科杂志》
CAS
CSCD
2004年第20期1568-1570,共3页
Orthopedic Journal of China
关键词
脊髓损伤
钙超载
原子吸收光谱分析法
内皮缩血管肽类
放射免疫法
Spinal cord injury
Calcium overload
Atomic absorption spectectomy
Vasoconstrictive peptide
Radio immunoassay
