Lescot T, Marchand-Verrecchia C, Puybasset L
Département d'anesthésie-réanimation, université Pierre et Marie-Curie, CHU de la Pitié-Salpêtrière, APHP, 47-83, boulevard de l'Hôpital, 75651 Paris cedex 13, France.
Ann Fr Anesth Reanim. 2006 Jul;25(7):755-60. doi: 10.1016/j.annfar.2006.03.014. Epub 2006 May 3.
Traumatic brain injury leads to primary and secondary brain injuries. Primary brain injury results from mechanical forces applied to the head at the time of impact. Secondary brain injury occurs at some time after the primary impact. Numerous pathophysiological mechanisms have been postulated to explain the progressive tissue damage produced by secondary injuries. The endogenous neuroinflammatory response after traumatic brain injury contributes to the development of blood-brain barrier breakdown, cerebral oedema and neuronal cell death and this has led to various pharmacological therapies to try to limit this type of damage. Studies employing glutamate receptor antagonist for cerebral protection have yielded promising results in laboratory animals but failed to produce clinically significant improvements. The present review will summarize the mechanisms of post traumatic cerebral inflammation with a special focus on the anti-inflammatory drug targets.
创伤性脑损伤会导致原发性和继发性脑损伤。原发性脑损伤是由撞击时施加于头部的机械力所致。继发性脑损伤发生在原发性撞击后的某个时间。人们已经提出了许多病理生理机制来解释继发性损伤所产生的渐进性组织损伤。创伤性脑损伤后的内源性神经炎症反应会促使血脑屏障破坏、脑水肿和神经元细胞死亡的发生，这也催生了各种旨在限制这类损伤的药物治疗方法。在实验动物中，使用谷氨酸受体拮抗剂进行脑保护的研究已取得了有前景的结果，但未能产生具有临床意义的改善。本综述将总结创伤后脑炎症的机制，特别关注抗炎药物靶点。
