Intratracheal Instillation of Surfactant Inhibits Lipopolysaccharide-induced Acute Respiratory Distress Syndrome in Rats

To determine the possible contribution of apoptosis in the pathogenesis of ARDS, we investigated the role of exogenous surfactant in a rodent model of ARDS after intratracheal instillation of lipopolysaccharide. Adult male Sprague Dawley rats were divided into four groups: buffer controls; rats challenged with LPS (055:B5 E.coli); challenged with LPS and treated with porcine surfactant (P-SF); and challenged with LPS and treated with synthetic surfactant (S-SF). Parameters of lung injury and inflammation were assessed 72h after treatment. We demonstrated that intratracheal administration of LPS could provoke significant lung injury, which was characterized by increase of MPO activity, wet/dry lung weight ratio, cytokine levels in bronchoalveolar lavage fluid (BALF), apoptosis of BALF cells and caspase-3 activity in lung tissue. Intratracheally delivered surfactant significantly reduced the parameters of LPS-induced inflammation: infiltration of inflammatory cells into lung tissue and BALF, pulmonary edema, lung myeloperoxidase activity, lipid peroxidation, caspase-3 activity, number of apoptotic BALF cells, lactate dehydrogenase level & pro-inflammatory cytokines levels. Taken together, the present data demonstrate that exogenous surfactant systemically attenuates lipopolysaccharide-induced inflammation.