Le Poncin-Lafitte M, Grosdemouge C, Roy-Billon C, Duterte D, Rapin J R
Rev Neurol (Paris). 1981;137(12):817-29.
Experimental microembolization of the rat brain has been used as a model for the production of cerebral microinfarction which resulted in a decrease in blood flow and secondary brain edema with changes in the oxidative metabolic pathways. The use of radioactive microspheres as embolizing agents allowed to determine the number of microinfarctions and their localization. In every microinfarct, oedema developed and it could be quantified by measuring the water percentage as soon as the fourth hour following the microembolization. The activity of oxygen-dependent enzymes was severely reduced in the ischemic area around which hyperemia was present. A quick decrease in the ATP and glucose levels and an increase in the lactate levels were observed, showing that the energetic metabolism was deviated towards the anaerobic pathway. On the fifth day following the microembolization, the oedema disappeared. The cellular metabolic activity and the cerebral blood flow almost returned to normal values within the same time. The simultaneously study of an avoidance response in a conditioned learning test showed a correlation between the reappearance of this response and the regression of the oedema.
大鼠脑实验性微栓塞已被用作产生脑微梗死的模型,这导致血流减少和继发性脑水肿,并伴有氧化代谢途径的变化。使用放射性微球作为栓塞剂能够确定微梗死的数量及其定位。在每个微梗死灶中都会出现水肿,并且在微栓塞后第四小时即可通过测量水分百分比对其进行量化。在存在充血的缺血区域周围,氧依赖性酶的活性严重降低。观察到ATP和葡萄糖水平迅速下降,乳酸水平升高,表明能量代谢转向无氧途径。微栓塞后第五天,水肿消失。细胞代谢活性和脑血流量几乎在同一时间恢复到正常水平。在条件学习测试中对回避反应的同时研究表明,这种反应的重新出现与水肿的消退之间存在相关性。