Jiang Min, Song Jun-Jie, Guo Xiao-Li, Tang Yong-Lin, Li Hai-Bo
Department of ICU-D, Second Affiliated Hospital of Harbin Medical University, Anesthesiology and Critical Medicine Major Laboratory of Heilongjiang Province, Harbin, Heilongjiang, China.
Respir Care. 2015 Dec;60(12):1720-8. doi: 10.4187/respcare.03640. Epub 2015 Sep 1.
Currently, no clinical or animal studies have been performed to establish the relationship between airway humidification and mechanical ventilation-induced lung inflammatory responses. Therefore, an animal model was established to better define this relationship.
Rabbits (n = 40) were randomly divided into 6 groups: control animals, sacrificed immediately after anesthesia (n = 2); dry gas group animals, subjected to mechanical ventilation for 8 h without humidification (n = 6); and experimental animals, subjected to mechanical ventilation for 8 h under humidification at 30, 35, 40, and 45°C, respectively (n = 8). Inflammatory cytokines in the bronchi alveolar lavage fluid (BALF) were measured. The integrity of the airway cilia and the tracheal epithelium was examined by scanning and transmission electron microscopy, respectively. Peripheral blood white blood cell counts and the wet to dry ratio and lung pathology were determined.
Dry gas group animals showed increased tumor necrosis factor alpha levels in BALF compared with control animals (P < .05). The tumor necrosis factor alpha and interleukin-8 levels in the BALF reached baseline levels when the humidification temperature was increased to 40°C. Scanning and transmission electron microscopy analysis revealed that cilia integrity was maintained in the 40°C groups. Peripheral white blood cell counts were not different among those groups. Compared with control animals, the wet to dry ratio was significantly elevated in the dry gas group (P < .05). Moreover, humidification at 40°C resulted in reduced pathologic injury compared with the other groups based on the histologic score.
Pathology and reduced inflammation observed in animals treated at 40°C was similar to that observed in the control animals, suggesting that appropriate humidification reduced inflammatory responses elicited as a consequence of mechanical ventilation, in addition to reducing damage to the cilia and reducing water loss in the airway.
目前,尚未进行临床或动物研究来确立气道湿化与机械通气诱导的肺部炎症反应之间的关系。因此,建立了一种动物模型以更好地明确这种关系。
将40只兔子随机分为6组:对照组动物,麻醉后立即处死(n = 2);干燥气体组动物,在无湿化的情况下进行8小时机械通气(n = 6);以及实验组动物,分别在30、35、40和45°C的湿化条件下进行8小时机械通气(n = 8)。测量支气管肺泡灌洗液(BALF)中的炎性细胞因子。分别通过扫描电子显微镜和透射电子显微镜检查气道纤毛和气管上皮的完整性。测定外周血白细胞计数、湿干比和肺病理学。
与对照组动物相比,干燥气体组动物的BALF中肿瘤坏死因子α水平升高(P < 0.05)。当湿化温度升至40°C时,BALF中的肿瘤坏死因子α和白细胞介素-8水平达到基线水平。扫描电子显微镜和透射电子显微镜分析显示,40°C组的纤毛完整性得以维持。这些组之间的外周白细胞计数没有差异。与对照组动物相比,干燥气体组的湿干比显著升高(P < 0.05)。此外,基于组织学评分,40°C湿化组与其他组相比,病理损伤减轻。
在40°C处理的动物中观察到的病理学变化和炎症减轻与对照组动物相似,这表明适当的湿化除了减少对纤毛的损伤和气道中的水分流失外,还减少了机械通气引起的炎症反应。