Dexmedetomidine Attenuates Acute Lung Injury Induced by Heatstroke and Improve Outcome

• Published in: Shock (Augusta, Ga.) Ga.), 2019-11, Vol.52 (5), p.532-539
• Main Authors: Geng, Yan, Li, Ru, He, Si-Xiao, Yang, Huo-Hong, Deng, Qiao-ting, Shao, Xiang-yang, Wu, Ying-song, Xu, Wei-wen, Ma, Qiang
• Format: Article
• Language: English
• ISSN: 1073-2322; 1540-0514
• DOI: 10.1097/SHK.0000000000001289

INTRODUCTION:Dexmedetomidine (DEX) has been demonstrated to inhibit inflammatory response and protect against multiorgan injury in various scenarios. The objectives of the present study were to ascertain whether DEX is able to attenuate acute lung injury (ALI) under heatstroke (HS), and to explore the underlying mechanism. METHODS:Male C57BL/6 mice were exposed to ambient temperature of 39.5 ± 0.2°C until core temperature reach 43°C. DEX or 0.9% saline was injected i.p. immediately. At the end of the experiment, bronchoalveolar lavage fluid (BALF) and lung tissue were harvested. RESULTS:HS induce ALI and pulmonary dysfunction, while DEX treatment could significantly inhibit lung injury and improve respiratory dysfunction under HS. The overall effect was beneficial and improved the 72 h cumulative survival rate of mice with HS. Furthermore, HS significantly elevated the levels of cytokines in BALF, as well as increased the activity of toll-like receptor 4 (TLR4)/MyD88/nuclear factor-κB (NFκB) signaling pathway in lung tissue, while DEX treatment could inhibit such effects. Finally, DEX could upregulate the expression of caveolin 1 downregulated by HS, which may contribute to the inhibition of TLR4/MyD88/NFκB signaling pathway. DISCUSSION:In conclusion, the present results indicated that DEX may protect against lung inflammatory response and injury under HS via TLR4/MyD88/NFκB signaling pathway, and caveolin-1 may participate in the effects.