To test this hypothesis, we explored the changes in Toll-like recetor 4 (TLR4), phosphorylated nuclear factor κB (p-NF-κB), Nuclear Factor κB (NF-κB), Hypoxia inducible factor-1α (HIF-1α), Galectin-3 (Gal-3), Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α) and NO in the embolic and non-embolic areas of the lung tissue in the rabbit APE combined with shock model. The gene discussed is TLR4; the disease is apparent mineralocorticoid excess.