TEMPORAL EVOLUTION AND SPATIAL-DISTRIBUTION OF THE DIFFUSION CONSTANT OF WATER IN RAT-BRAIN AFTER TRANSIENT MIDDLE CEREBRAL-ARTERY OCCLUSION

The regional distribution and temporal evolution of the diffusion coefficient (D(W)) of water in rat brain was measured during and after transient middle cerebral artery (MCA) occlusion. Male Wistar rats (n = 14) were subjected to 2 h of middle cerebral artery occlusion, induced by intracarotid insertion of a filament. Diffusion (n = 14) and perfusion (n = 7) weighted magnetic resonance imaging were performed before, and at various time points after MCA occlusion, ranging from 30 min up to 7 days. Our data demonstrate that the temporal profiles of D(W) differ between the severely and the least damaged regions of tissue. In the core of the lesion, where the tissue evolved to necrosis, D(W) declined significantly (P < 0.001) within 0.5 h after onset of ischemia, and remained depressed until 24 h after withdrawal of the suture. However, no statistically significant decline in D(W) was found in the perifocal regions containing morphologically intact cells. Perfusion MRI qualitatively exhibited a hypoperfusion and reperfusion during, and after 2 h MCA occlusion, respectively. A significant (r greater-than-or-equal-to 0.71, P < 0.01) correlation was found between DELTAD(W) (the difference in D(W) between the ipsilateral ischemic and homologous contralateral control regions) obtained immediately before withdrawal of the suture (2 h of ischemia) and at specific early time points after withdrawal of the suture, and the degree of ischemic cell damage. No significant (P > 0.01) correlation was detected at an early time points of ischemia or at other time points after withdrawal of the suture. Our data suggest that values for DELTAD(W) obtained at 2 h, during the period of MCA occlusion and at specific early time points after withdrawal of the suture, are highly correlated to the histological outcome of the tissue, and both DELTAD(W) and the temporal profile of D(W) may reflect underlying biophysical changes in the tissue evoked by the ischemic insult.