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Correlates between nuclear magnetic resonance spectroscopy, diffusion weighted imaging and CA1 morphometry following chronic brain ischemia
Author(s) -
de la Torre J. C.,
Butler K.,
Kozlowski P.,
Fortin T.,
Saunders J. K.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490410211
Subject(s) - ischemia , creatine , hippocampal formation , medicine , glial fibrillary acidic protein , brain ischemia , atrophy , magnetic resonance imaging , pathology , chemistry , radiology , immunohistochemistry
Chronic brain ischemia (CBI) was induced in aging (13 month) rats by ligating the left subclavian artery and placing temporary occluders in each common carotid artery [three‐vessel occlusion (3‐VO)]. Carotid artery occluders were removed after 1, 2, or 3 weeks following brain ischemia or maintained for 9 weeks. Two rats were kept with their occluders in place for 25 weeks. On weeks 3 and 9 after CBI, 31 P‐/ 1 H‐nuclear magnetic resonance (NMR) spectroscopy and high resolution diffusion weighted imaging were performed in vivo, non‐invasively for detection of hippocampal high energy phosphates, lactate, intracellular pH, N‐acetyl‐aspartate, choline, glutamate, creatine, and structural alterations of the brain following CBI. Brains were histologically processed for morphometry of glial fibrillary acidic protein (GFAP) and CA1 damaged neurons 9 weeks after CBI. 31 P‐/ 1 H‐NMR spectroscopy showed that high energy substrates remained normal in ischemic animals when compared to non‐ischemic controls except for an elevation of phosphomonoesters in the hippocampal region. Rats deoccluded 1 and 2 weeks after initiation of CBI had no NMR spectroscopic or imaging changes. Rats kept ischemic for 9 weeks showed high signal intensities in the parietal cortex detected by diffusion weighted imaging as well as CAI damage and increased GFAP density but no cortical atrophy or neuronal damage could be detected histologically. Rats kept ischemic for 25 weeks showed extensive cortical atrophy which corresponded to the high, signal intensity observed with diffusion weighted imaging in the group kept ischemic for 9 weeks. These findings indicate that NMR spectroscopy and difussion weighted imaging can be used to follow the progress of neuronal injury in vivo and non‐invasively. Moreover, diffusion weighted imaging may be an excellent predictor of cerebral damage and atrophy prior to histopatholog ical detection of such damage. Our present and previous findings using our 3‐VO model indicate that this aging rat model may be useful in screening potential therapy for neurodegenerative disorders associated with abnormal aging and memory impairment. © 1995 Wiley‐Liss, Inc.