ObjectiveTo observe the effects of cluster therapy combined with anisodamine, dexamethasone and ambroxol on arterial blood gas, inflammatory cytokines and pulmonary pathological changes by making an early (<48 h) primary blast lung injury model in rats. MethodsEighty Wistar rats were randomly divided into six groups, ie. a control group (n=5), an injury group (n=15), an ambroxol treatment group (n=15), a dexamethasone treatment group, a scopolamine treatment group (n=15), a combination of ambroxol, dexamethasone and anisodamine group (n=15). The treatment groups were injected intraperitoneally with ambroxol 46.7 mg/kg (three times a day) or (and) dexamethasone at 5 mg·kg–1·d–1 or (and) anisodamine at a dose of 3.33 mg/kg (three times a day). The rats in the injury group were injected intraperitoneally with an equal volume of normal saline. Respiratory rate and weight change were observed before and after injury. Five rats were sacrificed at 6 hours, 24 hours and 48 hours after injury in each experimental group. Arterial blood gas analysis, Yelverton pathological score, lung tissue wet/dry weight ratio, serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured. The lung histopathology was observed. ResultsAfter lung blast injury, the rats in the injury group showed progressive respiratory acidosis, and hypoxemia increased with the increase of IL-6 and TNF-α in a time-dependent manner. The PaO2 decreased in the groups with ambroxol, dexamethasone and anisodamine alone or in combination with anisodamine, and the contents of serum IL-6 and TNF-α decreased. Pathological edema and inflammatory infiltration of lung tissue were alleviated significantly. ConclusionsAfter treatment with dexamethasone, anisodamine and ambroxol after lung blast injury, blood gas analysis is improved, inflammatory factor level is decreased and lung injury is alleviated, indicating that the three drugs can treat lung detonation injury in rats. The cluster therapy is superior to the single drug therapy.
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.