Background and purpose: Baicalin has been reported to have anti-inflammatory effects and protect against various tissue injuries. However, the effect of baicalin on air embolism-induced acute lung injury has not been tested yet.
Experimental approach: Acute lung injury was induced by infusion of air at a rate of 0.25 mL.min(-1) for 1 min into the pulmonary artery of rat isolated lungs. At the end of the experiment, samples were collected for assessment of lung injury, biochemical analysis and histology. Different doses of baicalin (1, 2 and 4 mg.kg(-1)) were given into the perfusate before air infusion.
Key results: Air embolism elicited a significant increase in microvascular permeability (K(f)), lung weight gain, wet/dry weight ratio, pulmonary artery pressure and protein concentration in the bronchoalveolar lavage fluid. Levels of the cytokines, tumour necrosis factor alpha and cytokine-induced neutrophil chemoattractant-1 in perfusate, and malondialdehyde levels and myeloperoxidase activities in lung tissue were also significantly increased. In addition, histological examination showed increased neutrophil infiltration in lung tissues. Furthermore, nuclear factor-kappaB activity and degradation of IkappaB-alpha were significantly increased in lungs. Pretreatment of the lungs with baicalin (4 mg.kg(-1)) showed a statistically significant difference in all of the assessed parameters, except for alteration in the pulmonary artery pressure.
Conclusions and implications: Our study suggests that baicalin attenuated air embolism-induced acute lung injury and may be considered a useful adjunct drug therapy in this clinical condition.