Shiraishi K, Sharp F R, Simon R P
Department of Neurology, University of California, San Francisco.
J Cereb Blood Flow Metab. 1989 Dec;9(6):765-73. doi: 10.1038/jcbfm.1989.110.
The distribution and time course of altered cerebral metabolism following permanent focal ischemia was studied in rat using the 2-deoxyglucose (2DG) technique. Increased 2DG uptake preceded decreased 2DG uptake and infarction in the caudate putamen and cortex. Decreased 2DG uptake without infarction was observed for 72 h in thalamus and for 24 h in hippocampus (areas remote from the ischemic zones). This study supports the concept of cell excitation as a pathophysiologic process in permanent focal ischemia. The time course of increased metabolism may demarcate the time window of opportunity for the previously demonstrated attenuation of stroke size with inhibition of cell excitation by pharmacologic blockade of excitatory amino acid neurotransmission.
采用2-脱氧葡萄糖（2DG）技术在大鼠中研究了永久性局灶性缺血后脑代谢改变的分布及时间进程。尾状核壳核和皮质中2DG摄取增加先于2DG摄取减少和梗死形成。在丘脑观察到2DG摄取减少但无梗死持续72小时，在海马（远离缺血区的区域）观察到持续24小时。本研究支持细胞兴奋作为永久性局灶性缺血病理生理过程的概念。代谢增加的时间进程可能划定了先前证明的通过兴奋性氨基酸神经传递的药理学阻断抑制细胞兴奋来减小卒中体积的机会时间窗。
