高原失血性休克大鼠相关急性肺损伤病变及发病机制

发布时间：2018-03-24 09:02

  本文选题：失血性休克　切入点：高原　出处：《临床麻醉学杂志》2017年05期

【摘要】：目的探讨高原失血性休克相关急性肺损伤(acute lung injury,ALI)病变及发病机制。方法雄性Wistar大鼠72只,体重280~320g,随机分为六组:假手术组(Sham组)、休克15min组(HS15组)、休克30min组(HS30组)、休克45min组(HS45组)、休克60min组(HS60组)和休克90min组(HS90组),每组12只。建立高原大鼠失血性休克模型后,Sham组麻醉置管后不予失血,仅观察90min即刻处死,其余五组分别按照15、30、45、60和90min观察终止时间窗维持于休克状态。光镜下观察肺组织病理变化,测定肺湿/干重比(W/D)、计算肺通透指数,同时测定肺组织髓过氧化物酶(MPO)、总超氧化物歧化酶(T-SOD)的活性和丙二醛(MDA)的浓度,采用ELISA法检测肺组织中TNF-α和IL-10的浓度。采用免疫组化法检测肺组织中claudin-3和claudin-4的表达和分布。结果与Sham组比较,休克造成不同程度的肺损伤,且与休克维持时间成正比。在休克15~30min,大鼠肺组织W/D、肺通透指数、MPO、MDA、TNF-α、T-SOD和IL-10的变化甚微,在此之后,随着时间的延长,肺W/D、肺通透指数、MPO活性、MDA浓度和TNF-α浓度明显升高,同时伴随SOD活性和IL-10浓度的明显下降(P0.05)。claudin-3和claudin-4在肺上皮细胞和内皮细胞处的表达明显错位并减少(P0.05)。结论高原环境下,遭受失血性休克的大鼠血流动力学在短时间代偿后,病变呈现螺旋式恶化。且随着休克的延续,大鼠体内炎性/抗炎、氧化/抗氧化稳态失衡,导致肺上皮细胞内claudin-3和claudin-4流失,呈现出急性肺损伤的表现。
[Abstract]:Objective to investigate the pathological changes and pathogenesis of acute lung injury associated with hemorrhagic shock at high altitude. Methods 72 male Wistar rats were included in this study. Three groups, weighing 280 ~ 320g, were randomly divided into six groups: sham-operated group (Sham group), shock 15min group (HS15), shock 30min group (HS30), shock 45min group (HS45), shock 60min group (HS60) and shock 90min group (12 rats in each group). In the Sham group, no blood loss was observed after catheterization. The other five groups were killed immediately by observing 90min, and the other five groups were kept in shock state according to the observation time window of 15: 30 and 90min, respectively. The pathological changes of lung tissue were observed under light microscope, the wet / dry weight ratio of lung was measured and the lung permeability index was calculated. The activity of myeloperoxidase (MPO), total superoxide dismutase (T-SOD) and the concentration of malondialdehyde (MDA) in lung tissue were also determined. The concentrations of TNF- 伪 and IL-10 in lung tissue were detected by ELISA method, and the expression and distribution of claudin-3 and claudin-4 in lung tissue were detected by immunohistochemical method. Results compared with Sham group, shock caused different degree of lung injury. The lung permeability index (MPO) MDAA TNF- 伪 T-SOD and IL-10 in lung tissue of rats showed little change at 15: 30 min after shock. After that, the lung WR / D, pulmonary permeability index and TNF- 伪 concentration increased significantly with the prolongation of time. At the same time, the activity of SOD and the concentration of IL-10 decreased significantly. The expression of P0.05N. Claudin-3 and claudin-4 in pulmonary epithelial cells and endothelial cells were significantly mislocated and decreased. Conclusion under high altitude environment, the hemodynamics of rats suffering from hemorrhagic shock is compensated for a short time. With the continuation of shock, the inflammatory / anti-inflammatory, oxidative / antioxidant homeostasis in the body of rats resulted in the loss of claudin-3 and claudin-4 in lung epithelial cells, which showed the appearance of acute lung injury.
【作者单位】： 福建医科大学附属第二医院麻醉科;兰州军区兰州总医院麻醉手术科;
【基金】：全军面上基金课题(CLZ14L001) 兰州军区面上基金课题(CLZ12JB11)
【分类号】：R459.7

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