DYNAMICS OF CEREBRAL TISSUE-INJURY AND PERFUSION AFTER TEMPORARY HYPOXIA-ISCHEMIA IN THE RAT - EVIDENCE FOR REGION-SPECIFIC SENSITIVITY ANDDELAYED DAMAGE

Background and Purpose-Selective regional sensitivity and delayed dama ge in cerebral ischemia provide opportunities for directed and late th erapy for stroke. Our aim was to characterize the spatial and temporal profile of ischemia-induced changes in cerebral perfusion and tissue status, with the use of noninvasive MRI techniques, to gain more insig ht in region-specific vulnerability and delayed damage. Methods-Rats u nderwent 20 minutes of unilateral cerebral hypoxia-ischemia (HI). We p erformed combined repetitive quantitative diffusion-weighted, T2-weigh ted, and dynamic susceptibility contrast-enhanced MRI from before HI t o 5 hours after HI. Data were correlated with parallel blood oxygenati on level-dependent MRI and laser-Doppler flowmetry. Finally, MRI and h istology were done 24 and 72 hours after HI. Results-Severe hypoperfus ion during KI caused acute reductions of the apparent diffusion coeffi cient (ADC) of tissue water in the ipsilateral hemisphere. Reperfusion resulted in dynamic perfusion alterations that varied spatially. The ADC recovered completely within 1 hour in the hippocampus (from 0.68+/ -0.07 to 0.83+/-0.09x10(-3) mm(2)/s), cortex (from 0.56+/-0.06 to 0.77 +/-0.07x10(-3) mm(2)/s), and caudate putamen (from 0.58+/-0.06 to 0.75 +/-0.06x10(-3) mm(2)/s) but only partially or not at all in the thalam us (from 0.65+/-0.07 to 0.68+/-0.12x10(-3) mm(2)/s) and substantia nig ra (from 0.80+/-0.08 to 0.76+/-0.10x10(-3) mm(2)/s). Secondary ADC red uctions, accompanied by significant T2 elevations and histological dam age, were observed after 24 hours. Initial and secondary ADC decreases were observed invariably in the hippocampus, cortex, and caudate puta men and in approximately 70% of the animals in the thalamus and substa ntia nigra. Conclusions-Region-specific responses and delayed ischemic damage after transient Hr were demonstrated by MRI. Acute reperfusion -induced normalization of ADCs appeared to poorly predict ultimate tis sue recovery since secondary, irreversible damage developed eventually .