Intraventricular vascular endothelial growth factor antibody increases infarct volume following transient cerebral ischemia

AIM: To clarify the role of vascular endothelial growth factor (VEGF) in ne uronal damage induced by cerebral ischemia. METHODS: Expression of VEGF in adult rat brain was measured by immunohistochemistry. Transient middle cere bral artery occlusion (MCAO) model was induced by placing a nylon thread in the lumen of the internal carotid artery. The infarct volume was shown wit h 2,3,5-triphenyltetrazolium chloride (TTC) staining and quantitated by com puter image analyzer with and without VEGF antibody treatment. RESULTS: VEG F expression was widely distributed in neuronal cells besides vascular endo thelial cells, and the neuronal distribution of VEGF was specific. After in traventricular treatment with VEGF antibody (0.1 g.L-1 daily, for 7 d follo wing the ischemia), infarct volume in the antibody treatment was increased versus vehicle-treated rats [(21.6 +/- 2.1 vs 16 +/- 6) mm(3), P < 0.05] re spectively. CONCLUSION: Intraventricular injection of VEGF antibody increas ed the infarct volume after focal cerebral ischemia in rats, suggesting tha t expression of neuronal VEGF may be one of neuronal protective mechanisms.