ADHESION MOLECULES AND MICROVASCULAR CHANGES IN THE NONOBESE DIABETIC(NOD) MOUSE PANCREAS - AN NO-INHIBITOR (L-NAME) IS UNABLE TO BLOCK ADHESION INFLAMMATION-INDUCED ACTIVATION

The aim of the present study was to investigate the immunoreactivity o f pancreatic microvasculature with emphasis on the adhesion molecule e xpression in NOD mice at a very early stage and after tile start of in filtration, before the onset of the diabetic disease. Immunoreactivity for Ia-b, BM8 (mouse macrophages) and inter-cellular-adhesion-molecul e-1 (ICAM-1) molecules in untreated control mice and in animals treate d using an inhibitor of nitric oxide (NO) formation (L-arginine analog ue), as well as islet culture, nitrite assay and ultrastructural studi es were pet-formed. Results showed that Ia-b and ICAM-1 immunoreactivi ties on endothelia are a very early phenomenon and that pancreatic blo od vessels and, in particular, some peri-islet venules, as well as sev eral venules of the exocrine parenchyma, undergo significant morpholog ical changes, Several endothelial cells of both peri-islet and extra-i slet compartments, often showed Ia-b and ICAM-1 immunoreactivities, de monstrating that these I:ells are important for the adhesion processes taking place during early autoimmune inflammation. Inhibition of NO f ormation does not significantly affect ICAM-1 and 1a-b immunoreactivit y both ill vivo and in vitro, BM8 immunoreactive cells were considerab ly less in number although these were detected either around islets or along pancreatic seta, but rarely within the epithelial layer.