Analysis of evolutionary process of the tracheal and pulmonary injury by smoke inhalation in rodents

Abstract

The aim of this study was is to analyze the evolutionary process of lung and trachea by smoke inhalation injury in rodents. The study was conducted with 15 rats’ subjects to smoke inhalation through burning cotton during twenty-seven minutes inhaling smoke and one minute and thirty second inhaling air. Then, they receipted oxygen during thirty minutes. They were divided into 3 groups such as, control group (CG), group 24 hours (h) (G24), group 48 h (G48) and 72 h (G72). The animals were sacrificed 24, 48 and 72 h after the induction of inhalation injury and the CG was sacrificed in the same time of G24. Posteriorly, the tissues of the trachea and lungs were collected for analysis histological, malondialdehyde (MDA), sulfidril (SH), catalase (CAT), tumoral necrosis factor a (TNF- a), interleukin-1 ß (IL-1ß) analyses. The obtained results showed that smoke inhalation injury worsens the architecture of the trachea and lung due histological changes caused by intense inflammatory response (G24 and G48 of trachea and lung) triggering pulmonary edema (mainly G48 in lung) and, consequently, emphysema (G48 and G72 lung) and areas of fibrosis (G72 lung) when compared CG. Morover, the levels of TNF-a and IL-1ß were highs in trachea tissue, only in G24 with p=0.01 and p=0.00, respectively, when compared to CG. Besides, we also observed that oxidative stress high in all injured groups (G24, G48 and G72) with highs concentrations of levels serums of MDA (p=0.00) when compared to CG. However, we observed lows levels of SH in all injured groups in trachea (p=0.01) compared to CG, in comparison with levels of SH in lung tissue that no obtained difference significative (p=0.402). Also, lows levels of CAT in lung (p=0.02) in G24 compared to G48, G72 and CG. In this sample, exposure to smoke induced a focal, diffuse and acute inflammatory process in tracheal tissues on the respiratory epithelium, with loss of ciliated epithelial tissue, in addition to presenting interstitial and alveolar edemas and infiltrates of inflammatory cells in the pulmonary parenchyma in animals of experimental groups. Moreover, concomitant with the above changes, in the tracheal tissue, these alterations are also related to inflammatory cytokine activities (TNF and IL-1ß), which corroborates the action of oxidative stress.