Qian L, Ohno K, Maehara T, Tominaga B, Hirakawa K, Kuroiwa T, Takakuda K, Miyairi H
Department of Neurosurgery, Tokyo Medical and Dental University, Japan.
Acta Neurochir (Wien). 1996;138(1):90-8. doi: 10.1007/BF01411731.
We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an original midline fluid percussion injury device. Following different grades of trauma, lCBF was measured continuously in the right parietal cortex through a burr hole using laser Doppler flowmeter, and physiological parameters were monitored. Pathological changes also were evaluated microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pathophysiological response occurred after percussion pulses of less than 1.33 atmospheres (atm). In animals subjected to pulses of greater than 4.30 atm, lCBF increased synchronously with blood pressure, and then both parameters decreased continuously until death. In animals subjected to pulses of 1.53 to 2.33 atm, trauma produced a transient increase in lCBF with no synchronous rise in blood pressure. In animals subjected to pulses of 2.70 to 3.87 atm, lCBF increased synchronously with blood pressure immediately following the injury, but had decreased markedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The transient increase in lCBF occurred within 5 seconds following percussion pulses of greater than 1.53 atm and appeared to be independent of the rise in systemic blood pressure. Apnoea occurred in animals subjected to pulses of greater than 1.53 atm, and the duration of apnoea and mortality rate correlated with the magnitude of the applied injury. A power decrease in the electroencephalogram post-injury and a delay in its recovery, both depended on the magnitude of the injury with few regional differences in the beta-2 band power. The distribution and extent of blood-brain barrier disruption and small haemorrhages also correlated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma. The four patterns of lCBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.
我们使用一种原始的中线流体冲击损伤装置，研究了麻醉大鼠对流体冲击脑损伤的病理生理和形态学反应。在不同程度的创伤后，通过颅骨钻孔使用激光多普勒流量计连续测量右侧顶叶皮质的局部脑血流量（lCBF），并监测生理参数。还通过显微镜评估病理变化。在创伤后的最初2小时内，我们发现了四种脑循环反应模式。在冲击压力小于1.33个大气压（atm）的脉冲后，几乎没有可测量的病理生理反应。在受到大于4.30 atm脉冲作用的动物中，lCBF与血压同步升高，然后这两个参数持续下降直至死亡。在受到1.53至2.33 atm脉冲作用的动物中，创伤导致lCBF短暂升高，而血压没有同步升高。在受到2.70至3.87 atm脉冲作用的动物中，损伤后lCBF立即与血压同步升高，但在60秒时显著下降，并一直低于损伤前基线。血压在损伤后4分钟内恢复到基线。lCBF的短暂升高发生在大于1.53 atm的冲击脉冲后5秒内，并且似乎与全身血压的升高无关。在受到大于1.53 atm脉冲作用的动物中出现呼吸暂停，呼吸暂停的持续时间和死亡率与施加损伤的大小相关。损伤后脑电图功率降低及其恢复延迟，两者均取决于损伤的大小，在β-2频段功率方面几乎没有区域差异。血脑屏障破坏和小出血的分布及范围也与损伤的大小相关。中度创伤后2周，双侧海马中的神经元数量显著减少。本研究中显示的lCBF变化的四种模式以及对损伤的其他反应，可能有助于研究各种弥漫性脑损伤的分级模型。
