HYALURONAN IN RADIATION-INDUCED LUNG-DISEASE IN THE RAT

We have used a previously described model of bilateral radiation-induc ed lung disease in the rat (Ward et al., Radiat, Res., 136, 15-21, 199 3) to study the role of hyaluronan in this process. Hyaluronan was mea sured in the bronchoalveolar lavage fluid, serum and lung tissue of ra ts after gamma irradiation or sham irradiation. Four weeks after irrad iation, during peak alveolitis (12-fold increase in protein in the lav age, 7-fold increase in lavaged cells) hyaluronan was elevated 5.5-fol d in serum and 1.5-fold in the bronchoalveolar lavage fluid. Histochem ical staining demonstrated hyaluronan was in the intra-alveolar edema fluid but was not increased in the alveolar walls; hyaluronan, measure d by high-performance liquid chromatography, also was not elevated in lavaged lung tissue, Hyaluronan was not increased in bronchoalveolar l avage fluid, serum or lung tissue during pulmonary edema (2 weeks) or fibrosis (6 to 20 weeks). The administration of methylprednisolone sig nificantly decreased the alveolitis, including the increase in hyaluro nan in the alveolar space and serum, but did not suppress fibrosis. It appears that hyaluronan is a marker of inflammation and cannot be use d as a serum marker to predict the onset of radiation pneumonitis. Fur thermore, an increase in interstitial hyaluronan does not appear to be a necessary precursor in the evolution of radiation fibrosis. (C) 199 7 by Radiation Research Society.