A COMPARISON OF THE EARLY DEVELOPMENT OF ISCHEMIC BRAIN-DAMAGE IN NORMOGLYCEMIC AND HYPERGLYCEMIC RATS USING MAGNETIC-RESONANCE-IMAGING

The early evolution of ischemic brain injury under normoglycemic and s treptozotocin-induced hyperglycemic plasma conditions was studied usin g magnetic resonance imaging (MRI). Male Sprague-Dawley rats were subj ected to either permanent middle cerebral artery occlusion (MCAO), or l-h MCAO followed by reperfusion using the intraluminal suture inserti on method. The animals were divided into four groups each with eight r ats: normoglycemia with permanent MCAO, normoglycemia with l-h MCAO, h yperglycemia with permanent MCAO, and hyperglycemia with l-h MCAO. Dif fusion-weighted images (DWIs) and T2-weighted images (T2WIs) were aqui red every 1 h from 20 min until 6 h after MCAO, at which time cerebral plasma volume images (PVIs) were acquired. Tissue infarction was dete rmined by triphenyltetrazolium chloride staining at 7 h after MCAO. Th e ischemic damage, measured as the area of DWI and T2WI hyperintensity and tissue infarction, increased significantly in hyperglycemic rats in both permanent and transient MCAO models, In the permanent MCAO mod el, the maximal apparent water diffusion coefficient (ADC) decline und er either normo- or hyperglycemia was about 40%, but the speed of ADC drop was faster in hyperlgycemic rats than in normoglycemic rats. Repe rfusion after I h of MCAO in normoglycemic rats partly reversed the de cline in ADC, whereas the low ADC area continued to expand after reper fusion in the hyperlgycemic group. Between the two hyperglycemic group s with either permanent MCAO or reperfusion, no significant difference was found in the infarct volume measured at 7 h after MCAO, However, reperfusion dramatically increased the extent and accelerated the deve lopment rate of vasogenic edema. ADC in the hyperglycemic reperfusion group also dropped to a lower level. A large ''no-reflow'' zone was fo und in the ischemic hemisphere in the hyperglycemic reperfusion group, This study provides strong evidence to support that preischemic hyper glycemia exacerbates ischemic damage in both transient and permanent M CAO models and demonstrates, using MRI, that reperfusion under preisch emic hyperglycemia accelerates the evolution of early ischemic injury.