James H E, Schneider S, Bhasin S
Neurosurgery. 1987 Feb;20(2):219-21. doi: 10.1227/00006123-198702000-00003.
Experimental carbon dioxide brain lesions were created over the intact dura mater of the left parietooccipital region of the anesthetized albino rabbit (40-watt impacts of 0.5-second duration, for a total of 4 seconds, with 0.5-second intervals between impacts), and cerebral blood flow (CBF) studies were performed with the hydrogen clearance technique. The animals were mechanically ventilated to maintain a constant PaCO2. Blood pressure, central venous pressure, electroencephalogram, and intracranial pressure were continuously monitored. The control CBF before lesion was 64.1 +/- 15.8 and 70.9 +/- 13.4 ml/100 g/minute for the left and the right hemispheres, respectively. CBF studies at 2, 4, 6, 8, and 24 hours after the lesion did not significantly change from the control values, save for a trend to increase over the right hemisphere only at 2 hours (range 106.0 +/- 55.4 to 41.6 +/- 9.3). It is concluded that in this model the changes in intracranial pressure and brain edema that are seen and have been previously reported are not due to change in cerebral circulation. The brain edema that results probably has characteristics similar to those seen in the cryogenic lesion (vasogenic) model, and this could account for the rise in intracranial pressure.
在麻醉的白化兔左顶枕区完整硬脑膜上制造实验性二氧化碳脑损伤(使用40瓦,持续0.5秒,共4秒,每次冲击间隔0.5秒),并用氢清除技术进行脑血流量(CBF)研究。动物通过机械通气维持恒定的动脉血二氧化碳分压(PaCO2)。持续监测血压、中心静脉压、脑电图和颅内压。损伤前左、右半球的对照脑血流量分别为64.1±15.8和70.9±13.4毫升/100克/分钟。损伤后2、4、6、8和24小时的脑血流量研究与对照值相比无显著变化,仅在2小时时右半球有增加趋势(范围为106.0±55.4至41.6±9.3)。得出的结论是,在该模型中,先前报道的颅内压和脑水肿变化并非由于脑循环改变所致。由此产生的脑水肿可能具有与低温损伤(血管源性)模型中所见类似的特征,这可能是颅内压升高的原因。