OBJECTIVE: A rat model with chronic bronchitis was replicated by passive inhalation of cigarette smoking fume to study its long-term effects on lung injury and nitric oxide (NO), interluekin-6 (IL-6), interleukin-8 (IL-8). METHODS: Levels of nitrogen dioxide (NO(2)) and nitrogen trioxide (NO(3)) were measured with spectrophotometry in rats indicating their level of nitric oxide (NO). Levels of IL-6 and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Levels of NO in serum, bronchial alveolar lavage fluid (BALF) and lung tissue in the smoking group were significantly lower than those in the normal controls (P < 0.01). But, levels of IL-6 and IL-8 were higher in the smoking group than those in the controls. CONCLUSION: Long-term passive smoking could cause injury of lung tissue to certain extent, reduction in secretion of NO in endothelial cells and damage to pulmonary vessels.
OBJECTIVE: A rat model with chronic bronchitis was replicated by passive inhalation of cigarette smoking fume to study its long-term effects on lung injury and nitric oxide (NO), interluekin-6 (IL-6), interleukin-8 (IL-8). METHODS: Levels of nitrogen dioxide (NO(2)) and nitrogen trioxide (NO(3)) were measured with spectrophotometry in rats indicating their level of nitric oxide (NO). Levels of IL-6 and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Levels of NO in serum, bronchial alveolar lavage fluid (BALF) and lung tissue in the smoking group were significantly lower than those in the normal controls (P < 0.01). But, levels of IL-6 and IL-8 were higher in the smoking group than those in the controls. CONCLUSION: Long-term passive smoking could cause injury of lung tissue to certain extent, reduction in secretion of NO in endothelial cells and damage to pulmonary vessels.