Bures J, Koroleva V I, Korolev O S, Mares V
Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Zh Vyssh Nerv Deiat Im I P Pavlova. 1998 Jul-Aug;48(4):640-53.
The role of spreading depression (SD) in the development of ischemic brain damage in rats was studied in two models: focal cortical ischemia provoked by a photothrombotic occlusion of the middle cerebral artery (MCA) and systemic hypoxia induced by breathing with 0.8% carbon monoxide (CO). Spontaneous cortical SD waves occurring during illumination were found to delay the irreversible MCA occlusion. Thrombosis was probably prevented by episodes of striking vasodilation and hyperemia lasting for 1-2 min and accompanying every SD wave. The SD-induced hyperemia after permanent MCA occlusion seems to improve the oxygen supply of the penumbra zone. During hypoxia induced by one-hour respiration with 0.8% CO, COHb saturation of the blood reached 50-60%. SD waves occurred in different brain regions of lightly anesthetized rats (pentobarbital, 20 mg/kg) changed under the above conditions into prolonged depolarizations (HDs) which led to a substantial increase in animals' mortality (60%). The SDs evoked in the cortex and hippocampus of deeply anesthetized rats (pentobarbital, 50 mg/kg) showed that hippocampus became highly vulnerable by CO hypoxia. Duration of the SD-provoked HDs often reached 30-60 min after a single SD wave. Decreased cell density was found in CA1 area of the hippocampus 20-30 days after the CD-enhanced CO hypoxia. Cerebrolysin (2.5 ml/kg daily, during 10 days) prevented from severe hippocampal injury (formation of granulomas) usually seen in the left hemisphere of rats not treated with cerebrolysin.
在两种模型中研究了扩散性抑制（SD）在大鼠缺血性脑损伤发展中的作用：大脑中动脉（MCA）光血栓闭塞诱发的局灶性皮质缺血模型和吸入0.8%一氧化碳（CO）诱导的全身性缺氧模型。发现在光照期间出现的自发性皮质SD波会延迟MCA不可逆闭塞。每一次SD波伴随的持续1 - 2分钟的显著血管舒张和充血发作可能阻止了血栓形成。永久性MCA闭塞后由SD诱导的充血似乎改善了半暗带区域的氧气供应。在吸入0.8% CO进行一小时诱导缺氧期间，血液中碳氧血红蛋白（COHb）饱和度达到50 - 60%。在上述条件下，轻度麻醉大鼠（戊巴比妥，20 mg/kg）不同脑区出现的SD波转变为延长去极化（HDs），这导致动物死亡率大幅增加（60%）。在深度麻醉大鼠（戊巴比妥，50 mg/kg）的皮质和海马中诱发的SD表明，海马在CO缺氧时变得高度脆弱。单次SD波后，由SD诱发的HDs持续时间通常达到30 - 60分钟。在增强CO缺氧的SD后20 - 30天，海马CA1区细胞密度降低。脑活素（每天2.5 ml/kg，持续10天）可预防未用脑活素治疗的大鼠左半球通常出现的严重海马损伤（肉芽肿形成）。
