de la Torre J C, Butler K, Kozlowski P, Fortin T, Saunders J K
Division of Neurosurgery, University of New Mexico School of Medicine, Albuquerque 87131, USA.
J Neurosci Res. 1995 Jun 1;41(2):238-45. doi: 10.1002/jnr.490410211.
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, 31P-/1H-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. 31P-/1H-NMR spectroscopy showed that high energy substrates remained normal in ischemic animals when compared to non-ischemic controls except for an elevation of phosphomonesters 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 CA1 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.(ABSTRACT TRUNCATED AT 250 WORDS)
