Regulation of angiotensin Ⅱ type 2 receptor in mechanically ventilated lung injury
10.3760/cma.j.issn.1671-0282.2019.12.010
- VernacularTitle: 血管紧张素Ⅱ-2型受体激动剂在机械通气肺损伤时调控作用
- Author:
Shuangyong DONG
1
;
Han HAN
2
;
Yuansheng XU
1
;
Junfeng SONG
2
;
Zhenxi YU
2
;
Jin LI
2
;
Xuyang ZHENG
2
Author Information
1. Department of Emergency Medicine, Affiliated the First Hospital, School of Medicine, Zhejiang University, Hangzhou 310001, China
2. Department of Pediatrics, Affiliated the First Hospital, School of Medicine, Zhejiang University, Hangzhou 310001, China
- Publication Type:Journal Article
- Keywords:
Ventilator-induced lung injury;
AngiotensinⅡ- type 2 receptor agonist;
Alveolar macrophages;
Rats
- From:
Chinese Journal of Emergency Medicine
2019;28(12):1511-1516
- CountryChina
- Language:Chinese
-
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.
