You are here:
INCORPORATION OF LABELED NITRIC OXIDE INTO RESPIRATORY TRACT LINING FLUIDS AND BLOOD PLASMA DURING LUNG INFLAMMATION
Citation:
Slade, R., J. Norwood, K M. Crissman, J. L. McKee, AND G. E. Hatch. INCORPORATION OF LABELED NITRIC OXIDE INTO RESPIRATORY TRACT LINING FLUIDS AND BLOOD PLASMA DURING LUNG INFLAMMATION. Presented at American Thoracic Society, Seattle, WA, May 16-21, 2003.
Description:
Incorporation of labeled nitric oxide (N18O) into respiratory tract lining fluids and blood plasma during lung inflammation. Slade, R., Norwood, J., Crissman, K., McKee, J., Hatch, G. PTB, ETD, NHEERL, ORD, USEPA, Res. Tri. Pk., NC
Our earlier studies have demonstrated the incorporation of oxygen-18 labeled nitrogen dioxide (N18O2) into respiratory tract tissues and a potentiating effect of ascorbate deficiency. The present study sought to determine conditions which influence similar interactions of the lung with inhaled nitric oxide (N18O). We exposed guinea pigs (30 d old female Hartley) to 10 ppm N18O for 4 hr following intratracheal instillation of either lipopolysaccharide (LPS, 6.7 mg/kg) or zymosan (Z, 3.3 mg/kg) to initiate pulmonary inflammation. We also examined the effect of vitamin C deficiency (2 weeks prior). Results: 18O accumulation was detected in blood plasma, nasal lavage and bronchoalveolar lavage (BAL) of all N18O-exposed animals, but was rarely detectable in lung tissues. Z (but not LPS) enhanced plasma 18O following N18O exposure. In BAL fluid cell-free supernatant, some 18O incorporation was observed following N18O exposure, and both Z and LPS enhanced this incorporation (LPS increased it only in vitamin C deficient guinea pigs). The presence of lung inflammation was confirmed following Z and LPS by significant increases in BAL neutrophils. This inflammation was further enhanced by N18O in Z treated guinea pigs. Z (but not LPS) increased BAL protein, and N18O exposure tended to decrease this effect. In summary, we have shown that it is possible to detect incorporation of 18O into nasal lavage, BAL, and plasma following N18O exposure of guinea pigs, although this incorporation was much lower than we saw with N18O2. This 18O incorporation was enhanced by inflammation, but vitamin C status had only minimal effects. The incorporation of 18O that we detect is probably either the result of reactions of N18O with blood hemoglobin or superoxide anion produced by inflammatory cells. The binding of N18O during inflammation might provide a marker for in vivo inflammatory processes.
This abstract does not reflect EPA policy.