Kawakami S, Hossmann K A
J Neurol. 1977 Dec 1;217(1):31-42. doi: 10.1007/BF00316314.
Cerebral ischemia of 15 min was produced in rats by increasing intracranial pressure above the systolic blood pressure level by infusing artificial cerebrospinal fluid into the cisterna magna. Pulmonary edema was prevented by blocking the vasomotor response with a ganglioplegic agent, and reducing the fluid load by peritoneal dialysis. The EEG flattened after 10.1 +/- 1.5 sec. followed by a dilatation of the pupils after 1--2 min. The EEG began to recover in 21 of 32 rats after 8 to 35 min of recirculation. Spectral analysis revealed an initial return of slow waves and spindles followed by continuous fast frequency activity. The EEG did not recover or was secondarily suppressed in 12 animals after a few hours. Electrophysiological recovery depended on the cardiocirculatory and respiratory state, the recovery being optimal in animals with mild hypertension and a normal acid-base status of the blood.
通过向大鼠枕大池注入人工脑脊液使颅内压升高至收缩压水平以上，造成15分钟的脑缺血。使用神经节阻滞剂阻断血管运动反应，并通过腹膜透析减少液体负荷，以预防肺水肿。脑电图在10.1±1.5秒后变平，随后在1 - 2分钟后瞳孔散大。在32只大鼠中，21只在再灌注8至35分钟后脑电图开始恢复。频谱分析显示，最初是慢波和纺锤波恢复，随后是持续的快频率活动。12只动物在数小时后脑电图未恢复或继发抑制。电生理恢复取决于心脏循环和呼吸状态，在轻度高血压且血液酸碱状态正常的动物中恢复最佳。
