目的　建立一新的分级机械脑损伤动物模型。　方法　采用自行设计的撞击装置，以撞击峰压（ＰＰ）和形变（ＤＦ）作外力参数，并保持较恒定的撞压时间，观察４０ 只猫在不同撞击水平下的脑生理、病理变化和脑含水量。　结果　在低撞击水平（ＰＰ０ ．４５ ｋｇｃｍ２ ，ＤＦ２ ．５ ｍｍ） ，动物出现轻微脑损伤生理反应， 病理改变仅局限于撞压处的脑浅层，脑含水量不增加；在中度撞击水平（ＰＰ０．６５ ｋｇｃｍ２ ，ＤＦ３．５ ｍｍ）， 则出现明显脑损伤生理反应，脑病理改变达脑深部的基底节、海马和胼胝体，伤侧大脑半球含水量增加；在高撞击水平（ＰＰ０．８５ ｋｇｃｍ２ ，ＤＦ４．５ ｍｍ） ，脑损伤生理反应更明显，伤后出现血压下降，呼吸抑制，颅内压增高，脑病理改变广泛且深达脑干，双侧大脑半球含水量增加。　结论　该模型与临床加速型脑损伤机制相似，以峰压和形变作外力参数成功建立了分级机械脑损伤模型，该模型可重复性好，有助于分析不同程度脑损伤后继发病理生理变化的机制和进行相应的治疗研究。 Objective To establish a new animal model of graded mechanical brain injury. Methods A self-designed impact device was used to measure the peak pressure (PP) and deformation (DF) as the external force parameters and to maintain a constant pressure duration. The effects of brain stroke, brain pathology, Water content. Results At the low impact level (PP0.45 kgcm2, DF2.5 mm), the animals showed slight brain injury physiological responses. The pathological changes were only confined to the superficial cerebral plexus where the pressure was applied. The brain water content did not increase. (PP0.65 kgcm2, DF3.5 mm), there was a clear brain injury physiological response, brain pathology changes deep brain basal ganglia, hippocampus and corpus callosum, injured hemisphere hemisphere water content increased; high impact level ( PP0.85 kgcm2, DF4.5 mm). The physiological responses of brain injury were more obvious. After injury, the blood pressure dropped, respiratory depression and intracranial pressure increased. The brain pathology changed widely and deeply to the brain stem and bilateral cerebral hemispheres increase. Conclusions This model is similar to clinical accelerated brain injury. The models of mechanical brain injury were successfully established by using peak pressure and deformation as external force parameters. This model is reproducible and can be used to analyze the secondary pathophysiological changes after different degrees of brain injury Mechanism and conduct the corresponding treatment research.