Regulation of angiotensin II type 2 receptor in mechanically ventilated lung injury

Q4 Nursing

中华急诊医学杂志 Pub Date : 2019-12-10 DOI:10.3760/CMA.J.ISSN.1671-0282.2019.12.010

Dong Shuangyong, Han Han, Xu Yuansheng, Song Junfeng, Yu Zhen-xi, L. Jing, Zheng Xuyang

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Abstract

Objective Through the study of angiotensinⅡ- type 2 receptor agonist (AT2R) after pretreatment of mechanical ventilation lung injury (VILI) in rats model, to clarify the role of angiotensin Ⅱ - type 2 receptor agonist (C21) in alleviating VILI inflammation and the damage of immune function and its possible mechanism. Methods In this experiment, the acute lung injury model was established by mechanical spring-volume ventilation in SD rats, and C21 pretreatment was performed to observe the pathological condition of lung tissue in rats with different ventilation duration, and to detect the inflammatory changes of BALF lavage fluid. Flow cytometry was used to detect the CD68+/iNOS+ labeled M1 type AMφ and the CD68+/Arg-1+ labeled M2 type AMφ in alveolar lavage fluid. Results The mechanical VILI rat model was successfully established. The pathological injury score of the mechanical ventilation 4 h model, the wet/dry weight of lung tissue, the number of cells and protein in BALF lavage fluid were increased significantly, the levels of TNF-α and IL - 1 were increased significantly, the levels of IL-4 and IL-10 were decreased significantly, and the level of inflammatory reaction decreased with the increase of ventilation time. The M1/M2 ratio in the 4 h ventilation model group was the highest, which was significantly different from the control group (P<0.05). Compared to the model group, the C21 pretreatment significantly reduced the levels of proinflammatory factors TNF-αand IL-1, and increased the levels of anti-inflammatory factors IL-4 and IL-10 in BALF (P<0.01). After the intervention of AT2R agonist at 4 h, 6 h and 8 h, the M1/M2 ratio of the model was lower than that of the model without AT2R agonist at 4 h, 6 h and 8 h. Conclusion Mechanical ventilation for 4 h in SD rats can establish a mechanical ventilation lung injury model. AT2R agonist C21 can promote the polarization of macrophages to m2-type, and C21 pretreatment may alleviate VILI inflammation and immune damage by altering the polarization of macrophages. Key words: Ventilator-induced lung injury; AngiotensinⅡ- type 2 receptor agonist; Alveolar macrophages; Rats

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血管紧张素II型2受体在机械通气肺损伤中的调节作用

目的通过对大鼠机械通气性肺损伤（VILI）预处理后血管紧张素Ⅱ-2型受体激动剂（AT2R）的研究，阐明血管紧张素II-2型激动剂（C21）在减轻VILI炎症和免疫功能损害中的作用及其可能机制。方法采用弹簧容量机械通气法建立SD大鼠急性肺损伤模型，采用C21预处理，观察不同通气时间大鼠肺组织的病理状况，并检测BALF灌洗液的炎症变化。流式细胞仪检测肺泡灌洗液中CD68+/iNOS+标记的M1型AMφ和CD68+/Arg-1+标记的M2型AMφ。结果成功建立了机械性VILI大鼠模型。随着通气时间的增加，机械通气4h模型的病理损伤评分、肺组织湿重/干重、BALF灌洗液中细胞和蛋白质数量显著增加，TNF-α和IL-1水平显著升高，IL-4和IL-10水平显著降低，炎症反应水平降低。通气4 h模型组的M1/M2比值最高，与对照组有显著差异（P<0.05）。与模型组相比，C21预处理显著降低了BALF中促炎因子TNF-α和IL-1的水平，增加了抗炎因子IL-4和IL-10的水平（P<0.01）。AT2R激动剂干预4 h后，模型在4h、6h和8h的M1/M2比值均低于未加AT2R激动剂的模型。结论SD大鼠机械通气4h可建立机械通气性肺损伤模型。AT2R激动剂C21可以促进巨噬细胞向m2型的极化，C21预处理可以通过改变巨噬细胞的极化来减轻VILI炎症和免疫损伤。关键词：呼吸机致肺损伤；血管紧张素Ⅱ-2型受体激动剂；肺泡巨噬细胞；大鼠

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来源期刊

中华急诊医学杂志 Nursing-Emergency Nursing

CiteScore

0.10

自引率

0.00%

发文量

8629

期刊介绍： Chinese Journal of Emergency Medicine is the only national journal which represents the development of emergency medicine in China. The journal is supervised by China Association of Science and Technology, sponsored by Chinese Medical Association, and co-sponsored by Zhejiang University. The journal publishes original research articles dealing with all aspects of clinical practice and research in emergency medicine. The columns include Pre-Hospital Rescue, Emergency Care, Trauma, Resuscitation, Poisoning, Disaster Medicine, Continuing Education, etc. It has a wide coverage in China, and builds up communication with Hong Kong, Macao, Taiwan and international emergency medicine circles.