Effect of bilateral vagal nerves transection on the inflammatory reaction of rats induced by lung ischemia and reperfusion
10.11855/j.issn.0577-7402.2017.07.06
- VernacularTitle:双侧迷走神经切除对大鼠肺缺血再灌注损伤炎症反应的影响
- Author:
Wenjian WANG
;
Yan CHENG
;
Rurong WANG
- Keywords:
reperfusion injury;
lung injury;
inflammatory reaction;
vagus nerve
- From:
Medical Journal of Chinese People's Liberation Army
2017;42(7):608-611
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of bilateral vagal nerves transection on the inflammatory reaction of rats induced by lung ischemia and reperfusion.Methods Twenty-four adult male SD rats weighed 250-320g were randomly divided into 3 groups (8 each): Sham group (S group), ischemia reperfusion group (IR group) and bilateral vagal nerves transaction and ischemia-reperfusion group (NIR group). Blood gas analysis with arterial blood was performed to detect the arterial partial pressure of oxygen (PaO2) and arterial-alveolar oxygen pressure gradient (A-aDO2) before ischemia and 0.5 and 4 hours after reperfusion. At the end of the experiment, the left lung tissues were collected to measure wet/dry ratio, the pathological changes were observed by light microscopy, and inflammatory indicators, including tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) levels and myeloperoxidase (MPO) activity were detected.Results Compared with S group, ischemia and reperfusion injury sharply decreased PaO2 and increased A-aDO2; the MPO activity, the contents of TNF-α and IL-10 and the wet/dry ratio obviously increased in IR group; more infiltration of inflammatory cells, hemorrhage, thickening and swelling of alveolar walls were observed. Compared with IR group, PaO2 further decreased while A-aDO2 had no obvious change in NIR group, the inflammatory reaction and pathologic lesions in lung tissues were getting worse.ConclusionBilateral vagal nerves transaction may aggravate lung ischemia and reperfusion injury, suggesting that the integrity of vagal nerves play a significant role in regulating inflammatory reaction of lung ischemia and reperfusion injury in rats.
