• L F Wang, S Mehta, S Weicker, J A Scott, M Joseph, H M Razavi, and D G McCormack.
• A. C. Burton Vascular Biology Group, Lawson Health Research Inc., London, Ontario, N6A 4G5, Canada.
• Biochem. Biophys. Res. Commun. 2001 May 11;283(3):694-9.

AbstractAcute lung injury is an important feature of sepsis and increased iNOS expression and NO production contribute to the pathogenesis of this syndrome. We generated bone marrow-transplanted chimeric mice with iNOS expression limited to either inflammatory or pulmonary parenchymal cells, and assessed pulmonary iNOS activity and systemic levels of NO metabolites in an endotoxemic model of sepsis. We found that while both pulmonary parenchymal cells and inflammatory cells contribute to the increased lung iNOS activity in endotoxemia, pulmonary parenchymal cells contribute to a significantly greater degree. Using measurement of plasma NO(-)(x), whole body NO production was assessed in this model. We found that the main source of NO(-)(x) was again, parenchymal cells and not inflammatory cells. This is the first study to demonstrate that most of the increased NO production in this model of endotoxemic sepsis derives from parenchymal cells rather than inflammatory cells.Copyright 2001 Academic Press.

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