Hu Xin-gang, Ruan Xiang-cai, Yu Lin, Ding Ning, She Shou-zhang, Liao Yu-lin
Department of Anesthesiology, Guangzhou First Municipal People's Hospital Affiliated to Guangzhou Medical College, Guangzhou 510182, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2011 Jun;31(7):1252-5.
To investigate the effect of dexmedetomidine hydrochloride on inflammatory lung injury and phosphorylation of extracellular regulated protein (ERK1/2) in a rat model of ventilator-induced lung injury (VILI).
Thirty-six adult male SD rats were randomized into 3 groups (n=12) to receive a 4-h standard ventilation (group C, with tidal volume of 8 ml/kg and respiratory rate of 90/min), high-tidal volume ventilation (group H, with tidal volume of 20 ml/kg and respiratory rate of 50 /min), and high-tidal volume ventilation plus 0.5 µg·kg(-1)·h(-1) dexmedetomidine infusion (group D), with the maintenance of a positive end expiratory pressure (PEEP) of 0 cmH(2)O. After mechanical ventilation the rats were sacrificed to collect the lung lavage liquid and lung tissue to examine the pulmonary inflammatory changes and tumor necrosis factor-α (TNF-α) expression as well as the expressions of ERK1/2 and p-ERK1/2.
Groups H and D showed obvious lung injury and significant elevations of the total protein, WBC, MPO, TNF-α, and ERK1/2 phosphorylation as compared with those of group C. The rats in group D showed milder lung pathologies with significantly lower levels of phosphorylation of ERK1/2 and TNF-α compared with those in group H.
Dexmedetomidine can significantly attenuate VILI, decrease the production of the inflammatory molecules, and inhibit the activation of ERK1/2, demonstrating a protective effect against VILI.
探讨盐酸右美托咪定对呼吸机诱导性肺损伤（VILI）大鼠模型炎症性肺损伤及细胞外调节蛋白（ERK1/2）磷酸化的影响。
将36只成年雄性SD大鼠随机分为3组（n = 12），分别接受4小时的标准通气（C组，潮气量8 ml/kg，呼吸频率90次/分钟）、高潮气量通气（H组，潮气量20 ml/kg，呼吸频率50次/分钟）和高潮气量通气加0.5 μg·kg⁻¹·h⁻¹右美托咪定输注（D组），呼气末正压（PEEP）维持在0 cmH₂O。机械通气后处死大鼠，收集肺灌洗液和肺组织，检测肺部炎症变化、肿瘤坏死因子-α（TNF-α）表达以及ERK1/2和p-ERK1/2的表达。
与C组相比，H组和D组均出现明显的肺损伤，总蛋白、白细胞、髓过氧化物酶、TNF-α以及ERK1/2磷酸化水平显著升高。与H组相比，D组大鼠的肺部病变较轻，ERK1/2磷酸化水平和TNF-α水平显著降低。
右美托咪定可显著减轻VILI，减少炎症分子的产生，并抑制ERK1/2的激活，对VILI具有保护作用。
