Nedergaard M
Brain Res. 1987 Apr 7;408(1-2):79-85. doi: 10.1016/0006-8993(87)90360-x.
To study whether transient ischemia is influenced by hyperglycemia, the middle cerebral artery was occluded for 5, 10 and 15 min in normo- and hyperglycemic rats. Five-minute ischemia induced minor lesions in both groups. After 10-min ischemia a significant greater infarct volume was found in hyperglycemia compared with normoglycemia (29 +/- 9 mm3 vs 4 +/- 4 mm3, P less than 0.001). Fifteen-minute artery occlusion induced even more damage in both hyper- and normoglycemia (63 +/- 20 mm3 vs 13 +/- 12 mm3, P less than 0.006). The lateral part of striatum was infarcted in all hyperglycemic animals exposed to 10 or 15 min of ischemia. In the same area selective neuronal injury occurred in 6 out of 9 normoglycemic animals. The findings show that hyperglycemia increases brain damage during transient ischemia by conversion of selective neuronal injury into cerebral infarction.
为研究短暂性缺血是否受高血糖影响,在正常血糖和高血糖大鼠中,将大脑中动脉闭塞5、10和15分钟。5分钟的缺血在两组中均引起轻微损伤。缺血10分钟后,与正常血糖相比,高血糖组的梗死体积显著更大(29±9立方毫米对4±4立方毫米,P<0.001)。15分钟的动脉闭塞在高血糖和正常血糖组中均导致了更严重的损伤(63±20立方毫米对13±12立方毫米,P<0.006)。在所有经历10或15分钟缺血的高血糖动物中,纹状体外侧部分发生梗死。在9只正常血糖动物中的6只,同一区域出现了选择性神经元损伤。研究结果表明,高血糖通过将选择性神经元损伤转化为脑梗死,增加了短暂性缺血期间的脑损伤。