Dixon C E, Lyeth B G, Povlishock J T, Findling R L, Hamm R J, Marmarou A, Young H F, Hayes R L
J Neurosurg. 1987 Jul;67(1):110-9. doi: 10.3171/jns.1987.67.1.0110.
Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head injury.
液压冲击模型通过向颅腔内快速注入一定体积的液体来造成脑损伤。作者系统地研究了不同程度的液压冲击损伤对大鼠神经、全身生理和组织病理学变化的影响。急性神经学实验表明，53只大鼠的液压冲击损伤导致了不可逆的呼吸暂停和死亡，或者短暂的呼吸暂停（持续54秒或更短时间）以及姿势和非姿势功能的可逆性抑制（持续60分钟或更短时间）。随着损伤程度的增加，死亡率和躯体运动反射抑制的持续时间也增加。与其他通过撞击产生脑震荡损伤的大鼠模型不同，只有13%的幸存者出现惊厥。短暂的呼吸暂停可能与存活下来的动物所遭受的显著低氧损伤无关。10只遭受中度损伤（2.9个大气压）的大鼠表现出持续4至8天的慢性运动功能障碍。对20只大鼠进行的全身生理实验表明，所研究的所有损伤水平都会导致急性全身性高血压、心动过缓和血糖水平升高。较高程度的损伤会导致高血压随后出现低血压。高血压的持续时间和脑电图振幅抑制与损伤程度有关。低水平的损伤不会产生明显的组织病理学改变，而较高程度的损伤会导致蛛网膜下腔和脑实质内出血，并且随着存活时间的延长，会出现坏死性改变和空洞形成。这些数据表明，大鼠的液压冲击损伤再现了在其他模型和物种中观察到的许多头部损伤特征。因此，这种动物模型可能是研究与人类头部损伤类似的病理变化的一种有用的实验方法。
