| Role of Nitric Oxide in Lipopolysaccharide-Induced Acute Lung Injury and Lipid Peroxidation in Rats. |
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Kyoung Min Lee, Hee Uk Kwon, Kong Been Im, Jong Taek Park |
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Departments of Anesthesiology and Critical Care Medicine, Konyang University Medical School, Daejeon, Korea. kmlee@kyuh.co.kr |
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| Abstract |
BACKGROUND
Nitric oxide (NO) may act as an oxygen radical scavenger or as an antioxidant, and inhibit neutrophil superoxide anion production. In contrast, NO combines with superoxide to form peroxynitrite, a very damaging material whose decomposition RESULTS in the generation of a hydroxyl radical. This study was designed to determine the role of NO in the development of acute lung injury and lipid peroxidation induced by lipopolysaccharide (LPS) in rats.
METHODS
Male Sprague-Dawley rats (200 - 250 g) were given one of the following treatments; intraperitoneal normal saline 0.5 ml, intraperitoneal E. coli LPS (5 mg/kg) in 0.5 ml normal saline, 4 mg/kg L-N(6)-(1-iminoethyl)lysine (L-NIL) + LPS, or L-arginine (80 mg/kg) + LPS. Four hours after treatment, the rats were killed by an intraperitoneal pentobarbital injection (100 mg/kg) and plasma nitrate/nitrite concentration (Griess reagents) and lipid peroxide (LPO) concentration of the lung (Yagi's method) were measured (n = 8). In the other sets of experiments, myeloperoxidase activity of the lung (n = 5) and protein concentration of the bronchoalveolar lavage (BAL) fluid (BCA protein assay reagents, n = 4) were assayed.
RESULTS
LPS treatment increased plasma nitrate/nitrite concentrations approximately 6 times (20.9 1.8nM, P < 0.01) compared with the control group (3.6 +/- 0.7nM), and L-NIL treatment prevented this increase. L-NIL plus LPS treatment resulted in greater increase of LPO concentrations of the lung compared with the control (P < 0.05).
Myeloperoxidase activity and protein concentrations of BAL fluids were higher in LPS and L-NIL plus LPS treatment groups than the control group.
CONCLUSIONS
These results suggest that inhibition of the increase of NO by selective inducible NO synthase inhibitor L-NIL may increase lipid peroxidation in septic rats. |
| Key Words:
Animals: rats; Lung: acute lung injury; Toxicity: lipopolysaccharide; sepsis |
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