Figure 1.

Diameter changes in the experimental subgroups (A). Diameter changes of order 3 arterioles, expressed in percentage of baseline at the end of bilateral common carotid artery occlusion (BCCAO) and reperfusion (RE) in Sham-saline = sham operated subgroup; Hypo = hypoperfused subgroup; Hypo-M₁ = malvidin subgroup treated with lower dosage (9 mg/kg b.w.); Hypo-M₂ = malvidin subgroup treated with higher dosage (18 mg/kg b.w.); Hypo-L/M₂ = L-NIO (10 mg/kg b.w.) and higher dosage malvidin (18 mg/kg b.w.) subgroup. Data are reported as Mean ± SEM; ^§p < 0.01 vs. Baseline; °p < 0.01 vs. Sham-saline subgroup; *p < 0.01 vs. Hypo subgroup at the end of BCCAO; **p < 0.01 vs. Hypo subgroup at the end of RE; ⁺p < 0.01 vs. Hypo-M₂ subgroup at the end of BCCAO; ⁺⁺p < 0.01 vs. Hypo-M₂ subgroup at the end of RE. Computer-assisted images of a pial microvascular network under baseline conditions (B), at the end of BCCAO (C) and RE (D) in one of the hypoperfused rats. The increase in microvascular leakage is outlined by the marked change in the color of interstitium (from black to white). Computer-assisted images of a pial microvascular network under baseline conditions (E) at the end of BCCAO (F) and RE (G) in a higher dosage malvidin-treated rat (18 mg/kg b.w.), where there was nitric oxide (NO) leakage of fluorescent-dextran.