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Delayed changes in T 1 ‐weighted signal intensity in a rat model of 15‐minute transient focal ischemia studied by magnetic resonance imaging/spectroscopy and synchrotron radiation X‐ray fluorescence
Author(s) -
Wang Xuxia,
Qian Junchao,
He Rui,
Wei Li,
Liu Nianqing,
Zhang Zhiyong,
Huang Yuying,
Lei Hao
Publication year - 2006
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.20985
Subject(s) - ischemia , striatum , nuclear magnetic resonance , chemistry , magnetic resonance imaging , medicine , physics , dopamine , radiology
Previous studies have found that rats subjected to 15‐min transient middle cerebral artery occlusion (MCAO) show neurodegeneration in the dorsolateral striatum only, and the resulting striatal lesion is associated with increased T 1 ‐weighted (T 1 W) signal intensity (SI) and decreased T 2 ‐weighted (T 2 W) SI at 2–8 weeks after the initial ischemia. It has been shown that the delayed increase in T 1 W SI in the ischemic region is associated with deposition of paramagnetic manganese ions. However, it has been suggested that other mechanisms, such as tissue calcification and lipid accumulation, also contribute to the relaxation time changes. To clarify this issue, we measured changes in relaxation times, lipid accumulation, and elemental distributions in the brain of rats subjected to 15‐min MCAO using MRI, in vivo 1 H MR spectroscopy (MRS), and synchrotron radiation X‐ray fluorescence (SRXRF). The results show that a delayed (2 weeks after ischemia) increase in T 1 W SI in the ischemic striatum is associated with significant increases in manganese, calcium, and iron, but without evident accumulation of MRS‐visible lipids or hydroxyapatite precipitation. It was also found that 15‐min MCAO results in acutely reduced N‐acetylaspartate (NAA)/creatine (Cr) ratio in the ipsilateral striatum, which recovers to the control level at 2 weeks after ischemia. Magn Reson Med, 2006. © 2006 Wiley‐Liss, Inc.