目的　研制一减速性脑损伤实验动物模型。　方法　应用自行设计制造的撞击装置复制减速性脑损伤。撞击装置由转板、转轴、弹力带和支架 (撞砧 ) 4部分组成。实验共用兔 6 9只。其中预实验用兔 33只 ,建立撞击力与脑损伤程度间的关系 ;实验用兔 36只 ,分对照、轻伤、重伤 3组 ,每组 12只。观察兔脑损伤早期生理反应、病理改变、脑含水量和颅内压的变化。　结果　撞击后 ,动物均出现明显的脑损伤生理反应 ,包括伤后即刻血压骤升后骤降、呼吸变深快与呼吸暂停、疼痛反射抑制等 ,重伤组反应更剧烈。重伤组伤后 6h脑含水量明显增加 ,伤后 1～ 6h颅内压升高。撞击力在 (80 0± 5 0 )N以上时出现病理异常 ,病理脑损伤程度随撞击力上升而逐渐加重 ,在(110 0± 10 0 )N的重伤水平可见颅骨骨折、脑挫伤 (冲击伤和对冲伤 )、脑干损伤及硬膜下血肿等。当撞击力升至 (140 0± 15 0 )N以上时 ,动物多因呼吸骤停死亡。　结论　本实验颅脑损伤与临床减速性颅脑损伤机制类似 ,成功复制出临床颅脑损伤的多个重要特征。该模型将有助于对减速性脑损伤后的病理生理变化机制的更深入研究 ,以及对颅脑损伤的防护措施的研究和对重型颅脑损伤综合抢救治疗方案的探求 Objective To develop an experimental animal model of degenerative brain injury. Methods The impact device designed and manufactured by ourselves was used to replicate degenerative brain injury. Impact device by the transfer plate, shaft, elastic belt and bracket (striker anvil) 4 parts. The experiment shared 6 9 rabbits. Among them, 33 rabbits were used for pre-experiment to establish the relationship between the impact force and the degree of brain injury. Thirty-six rabbits were divided into control group, mild injury group and severe injury group of 12 rats. The changes of early physiological responses, pathological changes, brain water content and intracranial pressure were observed in rabbits with brain injury. Results After the impact, the animals showed obvious physiological responses to brain injury, including sharp plunge of blood pressure immediately after resuscitation, rapid respiration and apnea, and suppression of pain reflexes. Severe injuries were more severe. 6h after injury, the water content of brain in injured group increased obviously, and the intracranial pressure increased 1 ~ 6h after injury. Pathological abnormalities occurred when the impact force was over (80 0 ± 5 0) N, and the degree of pathological brain injury gradually increased with the increase of impact force. Skull fractures and brain contusion (impact injury) were observed at the level of (110 0 ± 10 0) N And hedge injury), brain stem injury and subdural hematoma. When the impact force rose to (140 0 ± 15 0) N above, animals died due to respiratory arrest. Conclusion The experimental craniocerebral injury is similar to the mechanism of clinical degenerative craniocerebral injury and successfully reproduces several important features of clinical craniocerebral injury. The model will help to further study the pathophysiological changes after degenerative brain injury, as well as the research on the protective measures of the brain injury and the exploration of the comprehensive treatment plan for the severe craniocerebral injury