| Objective Inhalation injury was the number one killer of burns patients, ang has high morbidity and mortalitiy. It can cause airway obstruction, atelectasis or lung collapse, eventually lead to respiratory failure. Tiotropium Bromide was a long-term M1and M3Muscarinic receptor antagonist, and widely used in the treatment of COPD and asthma stability for the expansion of bronchus and reduce mucus secretion, it can also inhibit the airway inflammation and remodeling. In this experiment, the model of smoke inhalation injury in rats was inhaled tiotropium,we explored the protective effect of Tiotropium Bromide on pulmonary of rats in smoke inhalation injury, through studying the pathological changes, inflammatory response and oxidation reaction of rat lung tissue.Method Fourty-two healthy male SD rats were randomly divided into3groups: sham group (n=10,not injured), control group (n=16, injured and not treated), treatment group (n=16, treated by tiotropium bromide), sham group was not injured, control group and treatment group were injured by smoke, at1hour after injury, the treatment group were treated by nebulization36μg of tiotropium bromide in3ml saline, control group received3ml saline during20minutes, repeated every8hours. At24hours after injury, rats were killed, blood were collected from abdominal aorta,after centrifugal, interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha were measured in serum; left lung was settlement by10%formaldehyde, pathology morphological observation was proceeded after section and stain; right lung was manufactured into homogenate by centrifuge, myeloperoxidase (MPO), malondialdehyde(MDA) and superoxide dismutase (SOD) were measured in the upper liquid. The numerical value was managed by statistical software, each mean was analyzed by single-factor ANOVA.Result1.General conditions:After inhalation injury, the rats appeared the symptoms of listlessness, respiratory and heart rate increasing, and they recovered gradually during resting for10minutes in open area.2. The macroscopic observation and pathological section of lung tissue:The lung tissue was pink, and there was no pulmonary congestion, edema or bleeding in sham group. Pulmonary congestion, edema, bleeding, and focal atelectasis were apparently displayed in control group, while these pathological changes in treatment group were lighten compared with control group, and these pathological changes were not found in sham group. H.E staining showed:the lungs of rats in the sham group had clear alveolar, complete construction, smooth alveolar walls, uniform alveolar interval, and there was no seepage or inflammatory cells in alveolar cavities. After injured by smoke, the lungs of rats displayed obvious pulmonary edema, seepage and bleeding, alveolar was broken, alveolar walls was thicken, focal atelectasis, mucus secretion and inflammatory cell seepage was displayed in alveolar cavities. These pathological changes were lighter in treatment group than in control group.3. the comparison of TNF-α, IL-6, IL-10in3groups:TNF-α、IL-6、IL-10was higher in control group and treatment group compared with sham group (P<0.01) TNF-α、IL-6was lower, IL-10was higher in treatment group than in control group (P <0.01)4.the comparison of MPO、MDA. SOD in3groups:MPO、MDA was higher, SOD was lower in control group and treatment group compared with sham group (P <0.01), MPO、MDA was lower, SOD was higher in treatment group than in control group (P<0.01)Conclusion Tiotropium bromide can reduce bronchial obstruction, lessen the incidence of atelectasis and (or) the pulmonary collapse, inhibit the release of promote inflammation factors IL-6, TNF alpha, promote the release of anti-inflammatory factor IL-10, reduce the damage of excessive inflammation to the body; it can also reduce the level of MDA and MPO, improve the SOD activity in injured lung tissue,as the role of the antioxidant. Therefore, tiotropium bromide can protect the pulmonary functions of rats with smoke inhalation injury。... |
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