本文選題：失血性休克　切入點：高原　出處：《臨床麻醉學雜志》2017年05期

【摘要】：目的探討高原失血性休克相關急性肺損傷(acute lung injury,ALI)病變及發(fā)病機制。方法雄性Wistar大鼠72只,體重280~320g,隨機分為六組:假手術組(Sham組)、休克15min組(HS15組)、休克30min組(HS30組)、休克45min組(HS45組)、休克60min組(HS60組)和休克90min組(HS90組),每組12只。建立高原大鼠失血性休克模型后,Sham組麻醉置管后不予失血,僅觀察90min即刻處死,其余五組分別按照15、30、45、60和90min觀察終止時間窗維持于休克狀態(tài)。光鏡下觀察肺組織病理變化,測定肺濕/干重比(W/D)、計算肺通透指數,同時測定肺組織髓過氧化物酶(MPO)、總超氧化物歧化酶(T-SOD)的活性和丙二醛(MDA)的濃度,采用ELISA法檢測肺組織中TNF-α和IL-10的濃度。采用免疫組化法檢測肺組織中claudin-3和claudin-4的表達和分布。結果與Sham組比較,休克造成不同程度的肺損傷,且與休克維持時間成正比。在休克15~30min,大鼠肺組織W/D、肺通透指數、MPO、MDA、TNF-α、T-SOD和IL-10的變化甚微,在此之后,隨著時間的延長,肺W/D、肺通透指數、MPO活性、MDA濃度和TNF-α濃度明顯升高,同時伴隨SOD活性和IL-10濃度的明顯下降(P0.05)。claudin-3和claudin-4在肺上皮細胞和內皮細胞處的表達明顯錯位并減少(P0.05)。結論高原環(huán)境下,遭受失血性休克的大鼠血流動力學在短時間代償后,病變呈現螺旋式惡化。且隨著休克的延續(xù),大鼠體內炎性/抗炎、氧化/抗氧化穩(wěn)態(tài)失衡,導致肺上皮細胞內claudin-3和claudin-4流失,呈現出急性肺損傷的表現。
[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- 偽 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- 偽 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- 偽 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.
【作者單位】： 福建醫(yī)科大學附屬第二醫(yī)院麻醉科;蘭州軍區(qū)蘭州總醫(yī)院麻醉手術科;
【基金】：全軍面上基金課題(CLZ14L001) 蘭州軍區(qū)面上基金課題(CLZ12JB11)
【分類號】：R459.7

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