TRPA1 ion channels in vagal afferent nerves contribute to ventilator-induced lung injury in a rat model.

In order to investigate the effects of transient receptor potential channel A1 (TRPA1)-mediated neurogenic inflammatory reaction on the process of ventilator-induced lung injury (VILI). A rat VILI model was created, and the TRPA1 selective antagonist, HC-030031, was used to investigate the role of TRPA1 in the process of VILI. 50 rats were randomly divided into five groups: vehicle group, low tidal volume group, high tidal volume group, low tidal volume group with TRPA1 inhibitor, high tidal volume group with TRPA1 inhibitor. Biochemical index of lung injury in each group were determined, including the W/D ratio, total protein, count of WBC, content of MDA, activities of MPO and SOD, content of IL-8, TNF-α and substance P. Results showed that TRPA1 inhibitor could significantly reduce the inflammatory response and generation of reactive oxygen species, improve SOD activity and inhibit the production of inflammatory factors in lung tissues. TRPA1 was expressed in vagal nerve afferents, and the TRPA1 antagonist significantly inhibited the expression of substance P, indicating the involvement of TRPA1 in neurogenic inflammation. In conclusion, TRPA1 might be involved in the pathophysiological process of VILI by inducing the neurogenic inflammation, and TRPA1 inhibitor could inhibit inflammatory response of VILI.