Els T, Röther J, Beaulieu C, de Crespigny A, Moseley M
Department of Neurology, Klinikum Mannheim, University of Heidelberg, Germany.
J Cereb Blood Flow Metab. 1997 May;17(5):591-5. doi: 10.1097/00004647-199705000-00015.
We investigated the effect of hyperglycemia on the initiation and propagation of spreading depression-like peri-infarct ischemic depolarization (SD) induced by focal cerebral ischemia in rats. Peri-infarct SD were monitored during the initial 15 minutes after remotely induced middle cerebral artery occlusion (MCAO) using serial diffusion weighted magnetic resonance imaging. Maps of the apparent diffusion coefficient (ADC) were calculated and ADC decreases were monitored over time. Hyperglycemic rats (n = 6) had a significant prolongation of the time from induction of MCAO to the start of the ADC decrease as compared with normoglycemic control rats. The time to the maximal ADC decrease was significantly delayed and recovery of transient ADC declines in the area adjacent to the ischemic core was significantly faster in hyperglycemic rats. We conclude that hyperglycemia delays the terminal depolarization in the ischemic core and supports a faster repolarization in severely mal-perfused penumbral tissue after SD, which reflects the increased availability of energy substrates in the state of hyperglycemia.
我们研究了高血糖对大鼠局灶性脑缺血诱导的梗死周围缺血性去极化(SD)样扩散性抑制的起始和传播的影响。在远程诱导大脑中动脉闭塞(MCAO)后的最初15分钟内,使用连续扩散加权磁共振成像监测梗死周围的SD。计算表观扩散系数(ADC)图,并随时间监测ADC的降低。与血糖正常的对照大鼠相比,高血糖大鼠(n = 6)从MCAO诱导到ADC降低开始的时间显著延长。高血糖大鼠ADC最大降低的时间显著延迟,缺血核心相邻区域短暂ADC下降的恢复明显更快。我们得出结论,高血糖会延迟缺血核心的终末去极化,并支持SD后严重灌注不良的半暗带组织更快地复极化,这反映了高血糖状态下能量底物可用性的增加。