摘要
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 。
Objective To set up an experimental animal model of head injury of deceleration. Methods The decelerating head injury was produced in rabbits by utilizing an impactor consisting of a rotor, elastic strips, a platform and a revolving board. Sixty nine rabbits were used in this experiment: 33 rabbits were for pre experiment to establish the correlation of impact force and brain damage, 36 rabbits were divided into a control group (n=12), a mild injury group (n=12) and a severe injury group (n=12) to elucidate the pathophysiological changes after head injury at different injury levels. Results The physiological responses after impact were observed in all traumatic animals, which showed a sudden rise or reduction of blood pressure, deep and fast breath and apnea, and pain reflects inhibition, etc. The responses were more obvious in the severe injury group than in the mild injury group. The water content of the brain increased 6 h after injury and the intracranial pressure went up 1 6 h after injury in the severe injury group. The pathological lesions were noted at or above the impact force level of (800±50) N. At the severe injury level of (1 100±100) N,there were almost all kinds of lesions, such as skull fracture, brain contusion ( coup injury and contre coup injury),brain stem injury and subdural hematoma. When the impact force rose to or over (1 400±150) N,the animals died of persistent apnea mostly. Conclusions A new practical and simple model of head injury of deceleration in rabbits has been developed with several features similar to the experience in the clinical setting. This model with the same biomechanical mechanism as the clinical head injury of deceleration is quite useful for further study of the pathophysiological mechanisms of head injury, safe measure of abating head injury and investigating the effective therapeutic method for severe head injuries.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2001年第4期212-215,共4页
Chinese Journal of Trauma
