Increased Brain Tumor Microvessel Permeability after Intracarotid Bradykinin Infusion Is Mediated by Nitric Oxide

摘要: Nitric oxide (NO), a free radical gas implicated in wide variety of biological reactions, is novel signaling molecule that may regulate vasodilation, cerebral blood flow, and vascular permeability. This study was performed to determine whether NO mediates the selective increase brain tumor microvessel permeability after intracarotid infusion bradykinin RG2 rat glioma model. Intracarotid selectively increased transport radiolabeled alpha-aminoisobutyric acid dextran into tumors. Transport normal not increased. The administration an synthase inhibitor, NG-nitro-L-arginine methyl ester, significantly inhibited tumors for both tracers. inhibitory effect ester on response reversed by L-arginine. expression two (NOS) isoforms cultured cell lines intracerebral examined immunohistochemistry Western blot analysis. High levels neuronal NOS were detected cells but tissue, except rare cells. endothelial form also expressed cells, as strongly expression. In gliomas, at higher than brain. These findings indicate gliomas express high NOS, which production NO, compared with We suggest microvessels mediated NO. Furthermore, absence account attenuated microvessels.