With the growth of offshore activities, the incidence rates of seawater drowning (SWD) induced acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) increase significantly higher than before. Pulmonary interstitial edema, alveolar septum fracture, red blood cells, and inflammatory cells infiltration can be seen under light microscope in the pathologic changes of lungs. The major clinical manifestations are continual hyoxemia and acidosis, which lead to a severe condition, a high death rate, and a poor treatment effect. Bone marrow mesenchymal stem cells are capable of self-renewal, multilineage differentiation and injured lung-homing, which are induced to differentiate into alveolar epithelial cells and pulmonary vascular endothelial cells for tissues repairing. This may be a new way to treat SWD-ALI and SW-ARDS.
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.
Seawater drowning leads to acute lung tissue structure injury, lung ventilation and air exchange dysfunction, acute pulmonary edema, and even acute respiratory failure. The pathogenesis of seawater induced acute lung injury is complex, involving inflammatory response, pulmonary edema, pulmonary surfactant, oxidative stress, apoptosis and autophagy. Timely and effective treatment is the key to reduce the mortality and disability rate of patients with seawater induced acute lung injury. This article summarizes the research progress in the pathogenic mechanism and treatment strategy of seawater induced acute lung injury, aiming to provide reference for the comprehensive treatment of seawater induced acute lung injury patients in clinical work and subsequent related research.