Nilsson B, Nordström C H
J Neurosurg. 1977 Aug;47(2):262-73. doi: 10.3171/jns.1977.47.2.0262.
Cerebral blood flow (CBF) and oxygen consumption (CMRO2) were determined during timmediate posttraumatic period in rats subjected to concussive impact acceleration. According to previous studies an impact of 9 m/sec velocity elicited typical and marked symptoms of experimental concussion and often a prolonged comatose state, accompanied by cerebral metabolic signs of energy failure. During the immediate concussive response there was an increase of the CBF, followed within the next few minutes by a decrease to about one-third of normal flow, and then by a tendency toward normalization of flow 20 to 40 minutes posttrauma. Simultaneous measurements of cerebral oxygen extraction indicated an increase of the CMRO2 during the first minute. During the ischemic phase oxygen extraction increased but the lowest CBF values were only partially compensated for, and normal oxygen availability could not be maintained. The combined data, including cerebrospinal fluid pressure measurements, indicated primary cerebrovascular effects of the concussive trauma. These vasomotor effects may induce critical cerebral ischemia and thus profoundly influence posttraumatic cerebral function, and cause irreversible damage.
在遭受冲击性撞击加速的大鼠创伤后即刻，测定其脑血流量（CBF）和氧耗量（CMRO2）。根据先前的研究，9米/秒速度的撞击会引发典型且明显的实验性脑震荡症状，并且常常伴有长时间的昏迷状态，同时伴有能量衰竭的脑代谢迹象。在即刻脑震荡反应期间，CBF增加，随后在接下来的几分钟内降至正常流量的约三分之一，然后在创伤后20至40分钟有流量趋于正常化的趋势。同时进行的脑氧摄取测量表明，在第一分钟内CMRO2增加。在缺血期，氧摄取增加，但最低的CBF值仅得到部分补偿，无法维持正常的氧供应。包括脑脊液压力测量在内的综合数据表明，脑震荡创伤具有原发性脑血管效应。这些血管运动效应可能诱发严重的脑缺血，从而深刻影响创伤后脑功能，并导致不可逆的损害。
