Truflandier Karine, Beaumont Eric, Maghni Karim, De Marchie Michel, Charbonney Emmanuel, Spahija Jadranka
Research Center, Sacré-Cœur Hospital of Montreal, Department of Medicine, Université de Montréal, Montreal, Quebec, Canada.
Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
Physiol Rep. 2016 Dec;4(24). doi: 10.14814/phy2.13009.
Mechanical ventilation (MV) is widely used in spinal injury patients to compensate for respiratory muscle failure. MV is known to induce lung inflammation, while spinal cord injury (SCI) is known to contribute to local inflammatory response. Interaction between MV and SCI was evaluated in order to assess the impact it may have on the pulmonary inflammatory profile. Sprague Dawley rats were anesthetized for 24 h and randomized to receive either MV or not. The MV group included C4-C5 SCI, T10 SCI and uninjured animals. The nonventilated (NV) group included T10 SCI and uninjured animals. Inflammatory cytokine profile, inflammation related to the SCI level, and oxidative stress mediators were measured in the bronchoalveolar lavage (BAL). The cytokine profile in BAL of MV animals showed increased levels of TNF-α, IL-1β, IL-6 and a decrease in IL-10 (P = 0.007) compared to the NV group. SCI did not modify IL-6 and IL-10 levels either in the MV or the NV groups, but cervical injury induced a decrease in IL-1β levels in MV animals. Cervical injury also reduced MV-induced pulmonary oxidative stress responses by decreasing isoprostane levels while increasing heme oxygenase-1 level. The thoracic SCI in NV animals increased M-CSF expression and promoted antioxidant pulmonary responses with low isoprostane and high heme oxygenase-1 levels. SCI shows a positive impact on MV-induced pulmonary inflammation, modulating specific lung immune and oxidative stress responses. Inflammation induced by MV and SCI interact closely and may have strong clinical implications since effective treatment of ventilated SCI patients may amplify pulmonary biotrauma.
机械通气(MV)广泛应用于脊髓损伤患者,以代偿呼吸肌衰竭。已知MV会诱发肺部炎症,而脊髓损伤(SCI)会导致局部炎症反应。为评估MV与SCI之间的相互作用对肺部炎症特征可能产生的影响,对其进行了评估。将Sprague Dawley大鼠麻醉24小时,随机分为接受MV组和未接受MV组。MV组包括C4 - C5脊髓损伤、T10脊髓损伤和未受伤的动物。非通气(NV)组包括T10脊髓损伤和未受伤的动物。在支气管肺泡灌洗(BAL)中测量炎症细胞因子谱、与SCI水平相关的炎症以及氧化应激介质。与NV组相比,MV组动物BAL中的细胞因子谱显示TNF-α、IL-1β、IL-6水平升高,IL-10水平降低(P = 0.007)。SCI在MV组和NV组中均未改变IL-6和IL-10水平,但颈椎损伤导致MV组动物IL-1β水平降低。颈椎损伤还通过降低异前列腺素水平同时增加血红素加氧酶-1水平,减轻了MV诱导的肺部氧化应激反应。NV组动物的胸椎SCI增加了M-CSF表达,并通过低异前列腺素和高血红素加氧酶-1水平促进了肺部抗氧化反应。SCI对MV诱导的肺部炎症有积极影响,调节特定的肺部免疫和氧化应激反应。MV和SCI诱导的炎症密切相互作用,可能具有重要的临床意义,因为有效治疗通气的SCI患者可能会加重肺部生物创伤。