title: [Effects of 7-nitroindazole on smoke inhalation pulmonary injury].
abstract: OBJECTIVE
  To investigate the effects of neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI) on smoke inhalation pulmonary injury in rats.
  
  
  METHODS
  Forty healthy male SD rats were randomly divided into three groups: control group (n=8), smoke inhalation model group (n=16) and 7-NI treatment group (n=16). After reproducing the smoke inhalation model, to the 7-NI treatment group rats 7-NI (20 mg/kg in 2 ml arachis oil) was administered by intraperitoneal injection, while in the control group and the model group, 2 ml arachis oil was administered by intraperitoneal injection. Arterial blood gas analysis was monitored at 2, 6, 12 and 24 hours. After rats were sacrificed, lung water was determined. The activities of super oxide dismutase (SOD), catalase (CAT), nitric oxide synthases (NOS), and the contents of tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO) were determined in pulmonary tissue homogenate. The pathological changes in pulmonary tissue were observed under light microscope.
  
  
  RESULTS
  Compared with model group, in 7-NI treatment group, arterial partial pressure of oxygen (PaO(2)) was elevated at each time point (all P<0.05), lung water was decreased (P<0.05). The activities of SOD and CAT were enhanced (all P<0.05), and the activities of nNOS and the content of NO were decreased (all P<0.05). TNF-alpha contents in lung tissues were decreased at 2 and 6 hours (both P<0.05). Pathological changes of less inflammatory cells infiltration and no punctate hemorrhage in lung interstitium in 7-NI treatment group than those in model group were seen under light microscope.
  
  
  CONCLUSIONS
  7-NI shows a good protective effect on smoke inhalation pulmonary injury, that it can raise PaO(2), increase the antioxidation ability, ameliorate lung edema and tissue inflammatory cells infiltration.
authors: Department of Respiratory Medicine, Tangdu Hospital, The Fourth Military Medical University, Xi'an, Shanxi, China. liuweilung@163.com
authors: Wei
authors: W
authors: Liu
authors: Fa-Guang
authors: FG
authors: Jin
authors: Gui-Sheng
authors: GS
authors: Qian
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D004195:Disease Models, Animal; D007191:Indazoles / Q000494:pharmacology*; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000037:antagonists & inhibitors*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015208:Smoke Inhalation Injury / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007191:Indazoles; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D013482:Superoxide Dismutase; C080122:7-nitroindazole