Nitric oxide as an inflammatory mediator of radiation pneumonitis
in rats.
Nozaki, Yasuhiro, Yoshinori Hasegawa, Akihide Takeuchi, Zuo-Heng Fan,
Ken-Ichi Isobe, Izumi Nakashima, Kaoru Shimokata.
First Department of Internal Medicine and Department of Immunology,
Nagoya University School of Medicine, Showa-ku, Nagoya, Japan.
Department of Immunology, National Institute for Longevity Sciences,
Ohbu, Aichi, Japan
APStracts 3:0232L, 1996.
Radiation pneumonitis is a major complication of radiation therapy. To
elucidate the mechanisms of radiation-induced pneumonitis, we studied
nitric oxide (NO) produced from lung tissues using a model of
unilaterally irradiated rats. Our results demonstrated that alveolar
macrophages (AM) produced NO after irradiation, and the expression of
inducible nitric oxide synthase in both AM and alveolar epithelial
cells was increased. Furthermore, the progression of radiation
pneumonitis was reduced with the in vivo treatment of nitric oxide
synthase inhibitor, L-NG-nitroarginine methyl ester (L-NAME). The
effect of L-NAME was further confirmed by the inhibition of m-RNA
expression for procollagen a1 type III of the lung. With these
results, NO produced from AM and alveolar epithelial cells after
irradiation may be an important mediator in the progression of
radiation pneumonitis.
Received 4 May 1996; accepted in final form 5 November 1996.
APS Manuscript Number L76-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996