Kofke W A, Garman R H, Stiller R, Rose M, Janosky J
Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh School of Medicine, PA 15261.
Brain Res. 1994 Jan 7;633(1-2):171-7. doi: 10.1016/0006-8993(94)91537-7.
We tested the hypothesis that hyperglycemic exacerbation of incomplete forebrain ischemia is mediated by increased extracellular dopamine levels. Normoglycemic and hyperglycemic Sprague-Dawley rats (eight each) with previously placed coaxial striatal microdialysis probes underwent 12 min of forebrain ischemia produced by bilateral carotid artery occlusion and trimethaphan-induced hypotension. Microdialysis was performed before, during, and for 6 h after ischemia, then perfusion-fixation was performed. Hyperglycemic rats had more severe postischemic damage in the caudate-putamen, neocortex, and hippocampus. Extracellular striatal dopamine levels were increased by ischemia, but were unaffected by hyperglycemia. These data show that hyperglycemic exacerbation of ischemic striatal damage does not depend on elevated extracellular dopamine levels.
我们检验了这样一个假设，即不完全性前脑缺血的高血糖加重是由细胞外多巴胺水平升高介导的。将预先植入同轴纹状体微透析探针的正常血糖和高血糖斯普拉格-道利大鼠（每组8只）通过双侧颈动脉闭塞和三甲噻芬诱导的低血压进行12分钟的前脑缺血。在缺血前、缺血期间和缺血后6小时进行微透析，然后进行灌注固定。高血糖大鼠在尾状核-壳核、新皮层和海马体中出现更严重的缺血后损伤。缺血使细胞外纹状体多巴胺水平升高，但不受高血糖的影响。这些数据表明，缺血性纹状体损伤的高血糖加重并不依赖于细胞外多巴胺水平的升高。
