Figure 5.

Evolution of the ischemic lesion from 1 hour to 24 hours after MCA occlusion in a rat treated with 0.9% saline (a) or rhVEGF₁₆₅ (b). Although areas of hyperintensity on the MRI were relatively similar at 1 hour of MCA occlusion in saline-treated (a) or rhVEGF₁₆₅–treated (b) rat, an area of hyperintensity on MRI was larger at 6 hours and 24 hours of ischemia in the rhVEGF-treated (b) rat compared with an area of hyperintensity at the same time points in the saline-treated rat (a). Differences of ischemic lesions observed on MRI between these two rats are confirmed on H&E-stained coronal sections obtained at 24 hours of ischemia (H&E) (a and b). Quantitative analysis of the ischemic area as a percentage of hemisphere measured on DWI at 6 hours and 24 hours of MCA occlusion (c) shows that ischemic areas are significantly (^AP < 0.05) larger in rats treated with rhVEGF₁₆₅ (solid line, n = 6) than in the control rats (dotted line, n = 7) at 6 hours and 24 hours of embolic MCA occlusion. Composite images (135 × 135 × 20 μm³) of microvessels (FITC-dextran, green) and MAP2 immunoreactivity (Cy5, red) show much less MAP2 immunoreactivity (red) in low plasma-perfused areas with extravasation of FITC-dextran (green) in the ipsilateral hemisphere (d) compared with the homologous tissue in the contralateral hemisphere (e) in a rat treated with rhVEGF₁₆₅ (1 hour) and sacrificed at 6 hours after MCA occlusion. Bar, 20 μm for d and e.