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用夹闭左颈外、枕、翼腭动脉，向左颈总动脉注射百日咳菌液（Ｐｖ）致大鼠急性脑水肿（ＢＥ），并同样注射生理盐水作对照。结果表明：注射ＰＶ后１５ｍｉｎ左侧脑组织水、蛋白、伊文思蓝（ＥＢ）含量明显高于对照组（Ｐ（０．０５），左脑半球出现蓝染，大脑皮质毛细血管周围星形肢质细胞突呈“小空泡”样变，内皮细胞内吞饮小泡增加，神经细胞无异常改变。注射ＰＶ６０ｍｉｎ大鼠舔吃、翻正反射消失。注射ＰＶ后２４０ｍｉｎ左、右侧脑水分、蛋白、ＥＢ含量均非常明显地高于对照组（Ｐ＜０．０１），脑蛋白与ＥＢ含量的增高呈正相关（ｒ＝０．９４４４），脑毛细血管周围垦形胶质细胞突呈大空泡或“水池”样变，神经元内线粒体肿胀，脊膜模糊或消失，并出现暗细胞。提示：本模型初为血脑屏障受损，继之神经细胞损害，同临床急性ＢＥ的发病相似。用本法建立的ＢＥ模型稳定、可靠、成功率高。
Acute cerebral edema (BE) was induced in rats by injection of pertussis bacilli (Pv) into the left common carotid artery with occlusion of the left neck, occipital and palatal arteries, and normal saline as a control. The results showed that the contents of water, protein and Evans blue (EB) in the left side of the left cerebral artery were significantly increased 15 min after the injection of PV, compared with the control group (P <0.05), blue staining in the left hemisphere, astrocytes After 60 min injection of PV, the content of water in the right cerebral side and the right side of the brain increased with the increase of endocytic vesical vesicles and no abnormal changes of nerve cells.After injection of PV60 min, Protein and EB were significantly higher than those in the control group (P <0.01). There was a positive correlation between brain protein and EB (r = 0.9444) Or “pool”, the mitochondria in the neurons swell, the dura obscure or disappear, and the dark cells appear.It is suggested that the model of the brain is impaired at the beginning of the BBB, followed by nerve cell damage, similar to the onset of clinical acute BE. BE model established by this method is stable, reliable and high success rate.