Objective To investigate the effects of ambroxol hydrochloride on surface structure of trachea mucosa in rats injured by intratracheally instilled amikacin. Methods Thirty Wistar rats injured by intratracheally instilled amikacin ( 0. 252 mL/kg) were randomly divided into a control group ( n =15) and an ambroxol group ( n= 15) . The rats in the ambroxol group were intraperitoneally injected with ambroxol hydrochloride ( 70 mg/kg) 5 minutes after amikacin administration. They were all equally divided into five subgroups and sacrificed at 2, 4, 8, 28, 48 hours respectively. Then the samples of 1/3 lower segment of trachea were collected and observed under scanning electron microscope. Results In the control group, the mucous secretion and its stickness were increased. The cilia were found lodged, sticked together, aligned abnormally, abrupt partly, and recovered slowly, with the percentage of damaged area of 98. 2% , 98. 5% , 97. 5%, 92. 7% , 82. 1% at 2, 4, 8,24,48 h, respectively. The injuries of mucosa in the ambroxol group were much milder and recovered more rapidly than those in the control group, with the percentage of damaged area of 85. 7% , 81. 9% , 73. 0% , 61. 9% , 50. 2% at 2, 4, 8, 24, 48 h, respectively. Conclusions Intratracheal instillation of amikacin can cause cilia ultrastructure damage on tracheal mucosa. Ambroxol can promote the recovery process and alleviate airway inflammation.
ObjectiveTo improve the seawater-drowning-induced lung injury model in rats, and investigate the protective effect of resveratrol against seawater-drowning-induced lung injury and its mechanism.MethodsA total of 112 SD healthy rats were randomly assigned into 5 groups: a control group (Group C, n=8), a seawater drowning group (Group S, n=32), a resveratrol prophylactic treatment group (Group S+R, n=32), a resveratrol group (Group R, n=8), and an endotracheal intubation group (Group E, n=32). A modified endotracheal intubation model was developed, and endotracheal intubation was used instead of tracheotomy. Blood gas analysis was performed on the abdominal aorta at each time point, then the rats were sacrificed to obtain their lungs. Lung wet-to-dry ratio (W/D), malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO) and cysteinyl aspartate specific proteinase (Caspase-3) were measured by enzyme linked immunosorbent assay. The histological sections of rat lungs were stained with haematoxylin-eosin. Groups S+R and R were pretreated with resveratrol (50 mg/kg) through intragastric administration for 3 days; then models were established and the rats were sacrificed 24 hours after the last intragastric administration.ResultsAfter seawater perfusion, arterial oxygen pressure decreased and arterial carbon dioxide pressure increased in blood gas analysis of rats, MDA content increased, MPO and SOD activity decreased, caspase-3 content and W/D ratio increased, as well as lung tissue pathological damage. The resveratrol pretreatment group showed the same change trend, but the damage degree was relatively light.ConclusionsSeawater perfusion can induce respiratory failure, pulmonary edema and hemorrhage in rats. Lung tissue apoptosis may occur when seawater submergence causes lung injury. Resveratrol pretreatment can ameliorate hypoxia and pulmonary edema in rats.