Selman W R, Ricci A J, Crumrine R C, LaManna J C, Ratcheson R A, Lust W D
Division of Neurosurgery, Case Western Reserve University, Cleveland, Ohio 44106.
Metab Brain Dis. 1990 Mar;5(1):33-44. doi: 10.1007/BF00996976.
Focal cerebral ischemia in the rat was induced by left middle cerebral artery occlusion. The area of ischemia was determined by infusion of a qualitative perfusion indicator, neutral red. The temporal evolution of alterations in regional energy metabolism was assessed by direct microquantitative histochemical analysis of high-energy phosphates, glucose, glycogen, and lactate content of the tissue. Perfusion analyses demonstrated a perifocal region of diminished, but not absent perfusion up to 6 hr after occlusion. By 24 hr, there was an abrupt demarcation between perfused and nonperfused regions. Profound metabolic alterations were seen as early as 20 min after occlusion. Although there was an area of intermediate metabolic derangement in the more medial portions of the lateral ipsilateral cortex up to 6 hr, by 24 hr there was an abrupt transition from normal to abnormal cortex. No evidence of metabolic recovery was seen in this model of permanent occlusion.
通过左侧大脑中动脉闭塞诱导大鼠局灶性脑缺血。缺血区域通过注入定性灌注指示剂中性红来确定。通过对组织中高能磷酸盐、葡萄糖、糖原和乳酸含量进行直接微量定量组织化学分析，评估区域能量代谢改变的时间演变。灌注分析表明，在闭塞后长达6小时，存在一个灌注减少但未完全缺失的灶周区域。到24小时时，灌注区域和非灌注区域之间出现了明显的分界。早在闭塞后20分钟就观察到了深刻的代谢改变。尽管在同侧外侧皮质更内侧部分，直至6小时都存在一个代谢紊乱的中间区域，但到24小时时，皮质从正常突然转变为异常。在这个永久性闭塞模型中未观察到代谢恢复的迹象。
