Protective effect of melatonin on reexpansion pulmonary edema in rats model.
- Author:
Ming ZHONG
1
;
Zhang-gang XUE
;
Jing CANG
;
Wei WU
;
Jun-feng HUANG
;
Du-ming ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cytokines; metabolism; Interleukin-8; metabolism; Lung; drug effects; metabolism; pathology; Male; Malondialdehyde; metabolism; Melatonin; therapeutic use; Nitric Oxide; metabolism; Oxidative Stress; drug effects; Peroxidase; metabolism; Pulmonary Edema; drug therapy; metabolism; pathology; Rats; Rats, Wistar
- From: Chinese Medical Journal 2013;126(3):500-504
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDRapid reexpansion of collapsed lungs leads to reexpansion pulmonary edema (RPE). We aimed to investigate the effect of melatonin in the prevention of RPE formation.
METHODSWe used a Wistar rat model in which the left lung was collapsed by ligating the left bronchus for 48 hours and then reexpanded and ventilated for an additional 2 hours. Thirty minutes before reexpansion, we injected melatonin (10 mg/kg) or vehicle intraperitoneally. We compared the wet/dry ratio, oxygenation index, myeloperoxidase (MPO) activity, nitric oxide (NO), malondialdehyde (MDA) and interleukin 8 (IL-8) levels in the reexpanded lungs between untreated and treated animals.
RESULTSWe found that the wet/dry ratio of the melatonin group was significantly lower than that of the vehicle group, and the oxygenation index was higher in the melatonin group. Compared with the control, melatonin pretreatment significantly decreased the activities of IL-8, NO, MDA levels and MPO in lung tissues. Histopathology of reexpanded lungs showed that the melatonin pretreatment group had less pulmonary edema and less inflammatory cell infiltration.
CONCLUSIONMelatonin decreases pulmonary edema and improves oxygenation after reexpansion by attenuating oxidative stress and inhibiting pro-inflammatory cytokines.