McIntosh T K, Vink R, Noble L, Yamakami I, Fernyak S, Soares H, Faden A L
Department of Surgery, University of Connecticut Health Center, Farmington 06032.
Neuroscience. 1989;28(1):233-44. doi: 10.1016/0306-4522(89)90247-9.
Experimental fluid-percussion models produce brain injury by rapidly injecting saline into the closed cranium. In the present study we characterize the physiological, histopathological and neurological responses to mechanical brain injury in the rat produced by lateral fluid-percussion injury of graded severity. Physiological experiments (n = 105) demonstrated that all levels of injury produced an acute and transient systemic hypertension and bradycardia. Acute hypertension followed by significant hypotension occurred at higher magnitudes of injury. Post-injury suppression of electroencephalographic amplitude was related to the severity of injury. An increase in slow wave (delta/theta) electroencephalographic activity with a concomitant decrease in alpha/beta electroencephalographic activity were observed only at moderate and high magnitude of injury and were correlated with a worsened neurological outcome (r = 0.84; P less than 0.05) and increased mortality (r = 0.66; P less than 0.05). Alterations in brainstem auditory-evoked potentials were also observed only at the higher levels of injury. Histopathological analysis revealed that the extent of post-injury hemorrhage, cavitation and vascular disruption (as measured by extravasation of Evans Blue dye) was greater at the higher magnitudes of injury. Neurological scoring performed over a 4-week post-injury period demonstrated that lateral fluid-percussion brain injury produces a chronic neurological deficit that is directly related to the severity of injury. Survival was also significantly reduced at the higher magnitudes of injury. These data demonstrate that the lateral model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may therefore be a useful experimental model for the study of the pathophysiology of traumatic brain injury.
实验性液体冲击模型通过向封闭的颅骨快速注入生理盐水来造成脑损伤。在本研究中，我们描述了大鼠因不同严重程度的侧方液体冲击损伤所导致的机械性脑损伤的生理、组织病理学和神经学反应。生理实验（n = 105）表明，所有损伤水平均产生急性和短暂的全身性高血压和心动过缓。在较高损伤程度时，会出现急性高血压后显著低血压的情况。损伤后脑电图振幅的抑制与损伤严重程度相关。仅在中度和高度损伤时观察到慢波（δ/θ）脑电图活动增加，同时α/β脑电图活动减少，且与神经学结果恶化（r = 0.84；P < 0.05）和死亡率增加（r = 0.66；P < 0.05）相关。仅在较高损伤水平时也观察到脑干听觉诱发电位的改变。组织病理学分析显示，在较高损伤程度时，损伤后出血、空洞形成和血管破坏的程度（通过伊文思蓝染料外渗测量）更大。在损伤后4周内进行的神经学评分表明，侧方液体冲击脑损伤会产生与损伤严重程度直接相关的慢性神经功能缺损。在较高损伤程度时，存活率也显著降低。这些数据表明，大鼠侧方液体冲击损伤模型重现了在其他模型和物种中观察到的许多头部损伤特征，因此可能是研究创伤性脑损伤病理生理学的有用实验模型。
