Increased microvascular permeability in early stage of dextran sulfate sodium-induced colitis: its interaction with lansoprazole binding sites

Clin Hemorheol Microcirc. 2006;34(1-2):193-9.

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.

MeSH terms

  • 2-Pyridinylmethylsulfinylbenzimidazoles
  • Animals
  • Binding Sites
  • Capillary Permeability / drug effects*
  • Colitis / chemically induced
  • Colitis / pathology*
  • Cytoplasm / metabolism
  • Dextran Sulfate
  • Goblet Cells / metabolism
  • Intestinal Mucosa / pathology
  • Lansoprazole
  • Macrophages
  • Neutrophils
  • Omeprazole / analogs & derivatives*
  • Omeprazole / pharmacokinetics
  • Proton Pump Inhibitors
  • Rats
  • Rats, Wistar

Substances

  • 2-Pyridinylmethylsulfinylbenzimidazoles
  • Proton Pump Inhibitors
  • Lansoprazole
  • Dextran Sulfate
  • Omeprazole