交感神经兴奋在外伤性脑水肿发生中的作用及机制

Role of sympathetic excitation in development of traumatic brain edema and its mechanism

目的 探讨交感神经兴奋在外伤性脑水肿发生中的作用 .方法 家兔 48只分成 A,B,C,D4组 ,采用自由落体脑损伤模型 ,致伤前对拟受伤侧颈交感神经进行不同处理 . A组 (n=12 )为假手术对照 ,仅显露神经 ;B组 (n=12 )为神经切断组 ,切断神经 ;C组 (n=12 )为神经刺激组 ,电刺激神经 ;D组 (n=12 )为切断后刺激组 ,切断神经后刺激该神经头端 .于伤后 2 h观察脑血管变化 ,2 4h观察脑组织 Evens blue(EB)含量 ,水及钠、钙含量 .结果 脑血管检查 B组伤区周围脑血管扩张瘀血 ,C组脑血管充盈不佳 ,D组与对照组差别不明显 .脑组织 EB含量 B组与 C组明显高于对照组 (P<0 .0 1) ,D组与对照组比较差别不显著 (P>0 .0 5 ) .脑组织水及钠、钙含量检测 ,B组与 C组亦明显高于对照组 (P<0 .0 1或 P<0 .0 5 ) ,D组与对照组比较差别不显著 (P>0 .0 5 ) .组织学检查表明 B组与 C组伤周脑组织水肿明显重于 D组和 A组 .结论 交感神经维持正常的兴奋性对脑有直接保护作用 ,而其过度兴奋则对脑有害 .交感神经兴奋性异常可能是外伤性脑水肿发生的一个原因 。

AIM To investigate the role of sympathetic excitation in traumatic brain edema. METHODS Forty eight rabbits were selected and divided into four groups: A, B, C, D. Head injuries were made by a dropping weight method. Before injury,the cervical sympathetic nerve (CSN) on the injury side was treated as follows: In group A ( n =12), CSN was only displayed which served as the control; in group B ( n =12), CSN was cut; in group C ( n =12), CSN was stimulated electrically; in group D ( n =12), CSN was cut plus stimulated on the upper end. Then cerebral blood vessels were examined at 2 h after injury,and cerebral contents of even blue (EB), water, natrium and calcium, were studied at 24 h after injury. RESULTS On cerebral vessel examination, the injured brain showed vessel dilated in group B, and poorly vessel perfused in group C, but no difference was found between group D and A. Cerebral EB contents increased in group B and C, which were significant compared with the control ( P < 0.01 ), but there was no statistical difference between group D and A ( P >0.05). Cerebral contents of water, natrium and calcium were significantly higher in group B and C than those in group A ( P <0.01 or P < 0.05 ), while there was no statistical difference between group D and A ( P >0.05). Histological examination proved that brain edema was severer in group B and C than in group D and A. CONCLUSION Maintenance of normal sympathetic excitation has protective effect on cerebral circulation and blood brain barrier, but excessive sympathetic irritation is harmful. Abnormal excitability of sympathetic nerve could be a causal factor of brain edema, and its mechanism might be that it leads to cerebral ischemia in the early peroid of trauma.