Experimental head injury in the rat. Part 3: Cerebral blood flow and oxygen consumption after concussive impact acceleration.
Experimental head injury in the rat. Part 3: Cerebral blood flow and oxygen consumption after concussive impact acceleration.
复制标题
大鼠实验性头部损伤。
作者：
B. Nilsson;C. Nordström
本实验测定了大鼠脑震荡冲击加速度伤后即刻的脑血流量（CBF）和氧耗量（CMRO_2）。根据以前的研究，9米/秒的速度的影响引起了典型的和明显的实验性脑震荡的症状，往往是一个长期的昏迷状态，伴随着能量衰竭的脑代谢体征。在脑震荡的即刻反应中，CBF增加，随后在接下来的几分钟内减少到正常流量的三分之一左右，然后在创伤后20至40分钟趋于正常化。脑氧摄取的同时测量表明在第一分钟期间CMRO 2增加。在缺血期氧摄取增加，但最低CBF值仅部分补偿，不能维持正常的氧可用性。综合数据，包括脑脊液压力测量，表明脑震荡创伤的主要脑血管影响。这些血管扩张效应可引起严重的脑缺血，从而深刻影响创伤后的脑功能，造成不可逆的损害。
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.