Cerebral blood flow and metabolic changes in hippocampal regions of a modified rat model with chronic cerebral hypoperfusion

被引:22
作者
Hai Jian [1 ]
Wu Yi-Fang [1 ]
Lin Qi [2 ]
Huang Xiao-Song [1 ]
Zhang Gui-Yun [1 ]
机构
[1] Tongji Univ, Tongji Hosp, Dept Neurosurg, Shanghai 200065, Peoples R China
[2] Shanghai Jiao Tong Univ, Inst Med Sci, Dept Pharm, Sch Med, Shanghai 200025, Peoples R China
基金
中国国家自然科学基金;
关键词
Animal model; Cerebral blood flow; Chronic cerebral hypoperfusion; Cognitive function; Hippocampus; H-1-MRS; MAGNETIC-RESONANCE-SPECTROSCOPY; OCCLUSION; BRAIN;
D O I
10.1007/s13760-012-0154-6
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Chronic cerebral hypoperfusion (CCH) causes neurodegeneration which contributes to the cognitive impairment. This study utilized a modified rat model with CCH to investigate cerebral blood flow (CBF) and hippocampal metabolic changes. CBF was measured by laser Doppler flowmetry. Various metabolic ratios were evaluated from selective volumes of interest (VOI) in left hippocampal regions using in vivo proton magnetic resonance spectroscopy (H-1-MRS). The ultrastructural changes with special respect to ribosomes in rat hippocampal CA1 neurons were studied by electron microscopy. CBF decreased immediately after CCH and remained reduced significantly at 1 day and 3 months postoperatively. H-1-MRS revealed that CCH led to a significant decrease of N-acetyl aspartate/creatine (NAA/Cr) ratio in the hippocampal VOI in the model rats compared with the sham-operated control rats. However, no changes of myo-inositol/Cr, choline/Cr and glutamate and glutamine/Cr ratios between the model and control groups were observed. Under electron microscopy, most rosette-shaped polyribosomes were relatively evenly distributed in the hippocampal CA1 neuronal cytoplasms of the control rats. After CCH, most ribosomes were clumped into large abnormal aggregates in the model rats. Our data suggests that both permanent decrease of CBF and reduction of NAA/Cr ratio in the hippocampal regions may be related to the cognitive deficits in rats with CCH.
引用
收藏
页码:313 / 317
页数:5
相关论文
共 20 条
[1]   Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: Implication in the pathogenesis of Alzheimer's disease [J].
Aliev, Gjumrakch ;
Gasimov, Eldar ;
Obrenovich, Mark E. ;
Fischbach, Kathryn ;
Shenk, Justin C. ;
Smith, Mark A. ;
Perry, George .
VASCULAR HEALTH AND RISK MANAGEMENT, 2008, 4 (03) :721-730
[2]   Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics [J].
de la Torre, JC .
LANCET NEUROLOGY, 2004, 3 (03) :184-190
[3]   Ribosomes and secretory granules in human mast cells: close associations demonstrated by staining with a chelating agent [J].
Dvorak, AM ;
Morgan, ES .
IMMUNOLOGICAL REVIEWS, 2001, 179 :94-101
[4]   CHANGES IN LOCAL CEREBRAL BLOOD-FLOW FOLLOWING BILATERAL CAROTID OCCLUSION IN SPONTANEOUSLY HYPERTENSIVE AND NORMOTENSIVE RATS [J].
FUJISHIMA, M ;
ISHITSUKA, T ;
NAKATOMI, Y ;
TAMAKI, K ;
OMAE, T .
STROKE, 1981, 12 (06) :874-876
[5]   THE CHARACTERISTICS OF LASER-DOPPLER FLOWMETRY FOR THE MEASUREMENT OF REGIONAL CEREBRAL BLOOD-FLOW [J].
FUKUDA, O ;
ENDO, S ;
KUWAYAMA, N ;
HARADA, J ;
TAKAKU, A .
NEUROSURGERY, 1995, 36 (02) :358-364
[6]   Vascular endothelial growth factor expression and angiogenesis induced by chronic cerebral hypoperfusion in rat brain [J].
Hai, J ;
Li, ST ;
Lin, Q ;
Pan, QG ;
Gao, F ;
Ding, MX .
NEUROSURGERY, 2003, 53 (04) :963-970
[7]   A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations [J].
Hai, J ;
Ding, MX ;
Guo, ZL ;
Wang, BY .
JOURNAL OF NEUROSURGERY, 2002, 97 (05) :1198-1202
[8]   Cognitive dysfunction induced by chronic cerebral hypoperfusion in a rat model associated with arteriovenous malformations [J].
Hai, Jian ;
Wan, Jue-Feng ;
Lin, Qi ;
Wang, Fei ;
Zhang, Lin ;
Li, Hui ;
Zhang, Lan ;
Chen, Yu-Ying ;
Lu, Yang .
BRAIN RESEARCH, 2009, 1301 :80-88
[9]   Protein folding - Molecular chaperones in the cytosol: from nascent chain to folded protein [J].
Hartl, FU ;
Hayer-Hartl, M .
SCIENCE, 2002, 295 (5561) :1852-1858
[10]   Co-translational protein aggregation after transient cerebral ischemia [J].
Liu, CL ;
Ge, P ;
Zhang, F ;
Hu, BR .
NEUROSCIENCE, 2005, 134 (04) :1273-1284