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Issue title: Selected Proceedings of the 6th Asian Congress for Mirocirculation (ACM'05) (Tokyo, February 25 and 26, 2005)
Article type: Research Article
Authors: Nakamura, Masahiko; | Asada, Maki | Matsui, Hidenori | Hibi, Norifumi | Tsuchimoto, Kanji | Inoue, Jun | Oda, Masaya
Affiliations: Center for Clinical Pharmacy and Clinical Sciences, School of Pharmaceutical Sciences, Kitasato University, Sanno Hospital, Tokyo, Japan | Kitasato Institute for Life Sciences & Graduate School of Infection Control Science, Kitasato University, Sanno Hospital, Tokyo, Japan | Department of Internal Medicine, School of Medicine, Keio University, Sanno Hospital, Tokyo, Japan | Organized Center of Clinical Medicine, International University of Health and Welfare and Department of Internal Medicine, Sanno Hospital, Tokyo, Japan
Note: [] Corresponding author. E-mail: [email protected].
Abstract: To clarify the microvascular changes and the effector sites of lansoprazole during the formation of colitis, the dextran sulfate sodium (DSS)-induced colitis was induced by the oral administration for 3 and 7 days. The alteration of the microvascular permeability was estimated by the intraaortic infusion of FITC-dextran. The effector sites of 3H-lansoprazole were examined by the intraaortic infusion of the radiolabelled compound and the autoradiographic procedure of water-soluble compounds. As a result, marked increase of the microvascular permeability was detected three days after DSS treatment near the inflammatory cells in the tip portion of the colonic mucosa. 3H-lansoprazole in the control rat colon was localized in the goblet cells, while in DSS-treated rats, 3H-lansoprazole was accumulated in the cytoplasm of the mesenchymal cells, and most of them coincided with polymorphonuclear leucocytes and macrophages.
Keywords: Dextran sulfate sodium, FITC-dextran, lansoprazole, autoradiography, colitis, neutrophil, macrophage
Journal: Clinical Hemorheology and Microcirculation, vol. 34, no. 1-2, pp. 193-199, 2006
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