VIRAL RESPIRATORY-INFECTION INCREASES ALVEOLAR MACROPHAGE CYTOPLASMICMOTILITY IN RATS - ROLE OF NO

Ingested ferrimagnetic (Fe3O4) particles were used to estimate noninva sively the motion of organelles in alveolar macrophages (AM) in intact rats during viral respiratory infection by parainfluenza type 1 (Send ai) virus. Four days after instillation of Fe3O4 particles (3 mg/kg) i nto the lung, remnant field strength (RFS) was measured at the body su rface immediately after magnetization of Fe3O4 particles by an externa lly applied magnetic field. RFS decreases with time, due to particle r otation (relaxation) which is related to cytoplasmic motility of AM. V iral infection increased the relaxation rate (lambda(0) per min), and increases in lambda(0) reached a maximum 3 days after nasal inoculatio n (day 3). Viral infection (day 3)-induced increases in lambda(0) were dose dependently inhibited by either the L-arginine analogue N-nitro- L-arginine or by methylene blue, an inhibitor of guanylate cyclase act ivity. Bronchoalveolar lavage fluid obtained from infected rats contai ned significantly higher levels of nitrite than that from control rats (P < 0.01). In in vitro experiments, AM from infected rats showed sig nificantly higher lambda(0), nitrite production, and intracellular gua nosine 3',5'-cyclic monophosphate levels than those from control rats (P < 0.01). Sodium nitroprusside, known to release nitric oxide concen tration dependently, increased lambda(0) of AM from noninfected rats i n vitro. These results suggest that nitric oxide plays an important ro le in AM cytoplasmic motility during viral respiratory infection.