AJP - Lung Cellular and Molecular Physiology, Vol 268, Issue 3 399-L406, Copyright © 1995 by American Physiological Society
Viral respiratory infection increases alveolar macrophage cytoplasmic motility in rats: role of NO
T. Fukushima, K. Sekizawa, M. Yamaya, S. Okinaga, M. Satoh and H. Sasaki
Department of Geriatric Medicine, Tohoku University School of Medicine, Sendai, Japan.
Ingested ferrimagnetic (Fe3O4) particles were used to estimate
noninvasively the motion of organelles in alveolar macrophages (AM) in
intact rats during viral respiratory infection by parainfluenza type 1
(Sendai) virus. Four days after instillation of Fe3O4 particles (3 mg/kg)
into the lung, remnant field strength (RFS) was measured at the body
surface immediately after magnetization of Fe3O4 particles by an externally
applied magnetic field. RFS decreases with time, due to particle rotation
(relaxation) which is related to cytoplasmic motility of AM. Viral
infection increased the relaxation rate (lambda o per min), and increases
in lambda o reached a maximum 3 days after nasal inoculation (day 3). Viral
infection (day 3)-induced increases in lambda o were dose dependently
inhibited by either the L-arginine analogue N-nitro-L-arginine or by
methylene blue, an inhibitor of guanylate cyclase activity. Bronchoalveolar
lavage fluid obtained from infected rats contained significantly higher
levels of nitrite than that from control rats (P < 0.01). In in vitro
experiments, AM from infected rats showed significantly higher lambda o,
nitrite production, and intracellular guanosine 3',5'-cyclic monophosphate
levels than those from control rats (P < 0.01). Sodium nitroprusside,
known to release nitric oxide concentration dependently, increased lambda o
of AM from noninfected rats in vitro. These results suggest that nitric
oxide plays an important role in AM cytoplasmic motility during viral
respiratory infection.
