Niacin attenuates acute lung injury induced by lipopolysaccharide in the hamster.

Lipopolysaccharide plays a major role in the development of lung injury induced by Gram-negative bacteria, but a protective agent to attenuate the LPS-induced lung injury has not been found. The aim of this study was to examine the effects of niacin on LPS-induced acute lung injury. We administered LPS (Escherichia coli) 0.01 mg.100 g-1 body weight, transtracheally into the lungs of hamsters. Niacin (250 or 500 mg.kg-1 body weight) was injected intraperitoneally 24 h before, and 1 h after the LPS administration. LPS treatment increased wet/dry lung weight, albumin content and neutrophil counts in bronchoalveolar lavage fluid. In hamsters treated with niacin, wet/dry lung weight, albumin content and intra-alveolar cell counts were normal. Nicotinamide adenine dinucleotide (NAD) was significantly decreased in lung tissue of hamsters treated with LPS alone, but was increased in hamsters treated with LPS and niacin. Histopathological examination revealed that niacin-treated LPS-administered hamsters had lungs with no or occasional inflammatory cell infiltration in alveolar spaces, in contrast to the lungs of LPS-treated hamsters, which were infiltrated with numerous inflammatory cells. We conclude that niacin attenuates LPS-induced acute lung injury, probably, in part, by preventing the depletion of NAD.