Uncoupling of local cerebral glucose metabolism and blood flow after acute fluid-percussion injury in rats
Uncoupling of local cerebral glucose metabolism and blood flow after acute fluid-percussion injury in rats
复制标题
DOI：
10.1152/ajpheart.1997.272.6.h2859
复制
发表时间：
1997-06-01
影响因子：
4.8
通讯作者：
Busto, R
中科院分区：
文献类型：
--
作者：
Ginsberg, MD;Zhao, W;Busto, R
我们评估了局部脑葡萄糖代谢（lCMR（Glc））和血流量（ICBF）的相互关系，在第一个小时后，在大鼠脊髓旁液压冲击头损伤（FPI）。分别用2-[C-14]脱氧葡萄糖和C-14-标记的碘安替比林对lCMR（Glc）和lCBF的匹配系列进行放射自显影研究。三维放射自显影图像映射用于生成平均数据集，从中导出平均lCMR（Glc）与lCBF比率数据集。与假手术FPI大鼠相比，创伤同侧新皮层区域的lCBF平均降低了44%，而对侧lCBF值没有改变。相比之下，ICMR（葡萄糖）在两个半球的许多皮质和皮质下部位升高;这相当于丘脑新皮质区增加1.3至1.4倍，海马增加1.6至1.7倍。lCMR（Glc）与lCBF比值数据显示FPI同侧（P = 7 x 10（-7））和对侧（P = 0.003）均显著升高。代谢流解偶联的程度，平均而言，在同侧海马和新皮质达到2.5倍，对侧达到1.7倍。明显的代谢流解离的位点密切对应于先前记录的神经元坏死的组织学分布。我们的研究结果类似于急性局灶性缺血半暗带发生的事件，并表明类似的损伤机制可能是有效的。
We assessed local cerebral glucose metabolism (lCMR(Glc)) and blood flow (ICBF) interrelationships in the first hour after parasagittal fluid-percussion head injury (FPI) in rats. Matched series were studied autoradiographically for lCMR(Glc) and lCBF with 2-[C-14]deoxyglucose and C-14-labeled iodoantipyrine, respectively. Three-dimensional autoradiographic-image mapping was used to generate average data sets from which a mean lCMR(Glc)-to-lCBF ratio data set was derived. lCBF in neocortical regions ipsilateral to the trauma were depressed, on average, by 44% compared with sham-FPI rats, whereas contralateral lCBF values were not altered. By contrast, lCMR(Glc) was elevated in many cortical and subcortical sites of both hemispheres; this amounted to 1.3- to 1.4-fold increases in neocortical regions in the thalamus and 1.6- to 1.7-fold increases in the hippocampus. The lCMR(Glc)-to-lCBF ratio data revealed striking elevations both ipsilateral (P = 7 x 10(-7)) and contralateral to the FPI (P = 0.003). The extent of metabolism-flow uncoupling, on average, amounted to 2.5-fold in the ipsilateral hippocampus and neocortex and 1.7-fold contralaterally. The loci of pronounced metabolism-flow dissociation corresponded closely to the previously documented histological distribution of neuronal necrosis. Our findings resemble events occurring in the acute focal ischemic penumbra and suggest that similar injury mechanisms may be operative.