ABSTRACT
The effect of low-level laser therapy (LLLT) on an experimental model of ventilator-induced lung injury (VILI) was evaluated in this study. 24 adult Wistar rats were randomized into four groups: protective mechanical ventilation (PMV), PMV + laser, VILI and VILI + laser. The animals of the PMV and VILI groups were ventilated with tidal volumes of 6 and 35 ml kg-1, respectively, for 90 minutes. After the first 60 minutes of ventilation, the animals in the laser groups were irradiated (808 nm, 100 mW power density, 20 J cm-2 energy density, continuous emission mode, and exposure time of 5 s) and after 30 minutes of irradiation, the animals were euthanized. Lung samples were removed for morphological analysis, bronchoalveolar lavage (BAL) and real time quantitative polynucleotide chain reaction (RT-qPCR). The VILI group showed a greater acute lung injury (ALI) score with an increase in neutrophil infiltration, higher neutrophil count in the BAL fluid and greater cytokine mRNA expression compared to the PMV groups (p < 0.05). The VILI + laser group when compared to the VILI group showed a lower ALI score (0.35 ± 0.08 vs. 0.54 ± 0.13, p < 0.05), alveolar neutrophil infiltration (7.00 ± 5.73 vs. 21.50 ± 9.52, p < 0.05), total cell count (1.90 ± 0.71 vs. 4.09 ± 0.96 × 105, p < 0.05) and neutrophil count in the BAL fluid (0.60 ± 0.37 vs. 2.28 ± 0.48 × 105, p < 0.05). Moreover, LLLT induced a decrease in pro-inflammatory and an increase of anti-inflammatory mRNA levels compared to the VILI group (p < 0.05). In conclusion, LLLT was found to reduce the inflammatory response in an experimental model of VILI.
Subject(s)
Disease Models, Animal , Inflammation/therapy , Low-Level Light Therapy , Ventilator-Induced Lung Injury/therapy , Animals , Male , Rats , Rats, WistarABSTRACT
The response of lungs with emphysema to an acute lung injury (ALI) remains unclear. This study compared the lung response to intratracheal instillation of lipopolysaccharide (LPS) in rats with and without emphysema. Twenty-four Wistar rats were randomized to four groups: control group (C-G), ALI group (ALI-G), emphysema group (E-G), emphysema and ALI group (E-ALI-G). Euthanasia and the following analysis were performed 24 h after ALI induction: lung histology, bronchoalveolar lavage (BAL), mRNA expression of inflammatory mediators, and blood gas measures. The histological analysis showed that animals of ALI-G (0.55 ± 0.15) and E-ALI-G (0.69 ± 0.08) had a higher ALI score compared to C-G (0.12 ± 0.04) and E-G (0.16 ± 0.04) (p < 0.05). The analysis of each component of the score demonstrated that ALI-G and E-ALI-G had greater alveolar and interstitial neutrophil infiltration, as well as greater amount of alveolar proteinaceous debris. Comparing the two groups that received LPS, there was a trend of higher ALI in the E-ALI-G, specially due to a higher neutrophil infiltration in the alveolar spaces and a higher septal thickening. Total cell count (E-G = 3.09 ± 0.83; ALI-G = 4.45 ± 1.9; E-ALI-G = 5.9 ± 2.1; C-G = 0.73 ± 0.37 × 105) and neutrophil count (E-G = 0.69 ± 0.35; ALI-G = 2.53 ± 1.09; E-ALI-G = 3.86 ± 1.4; C-G = 0.09 ± 0.07 × 105) in the BAL were higher in the groups E-G, ALI-G, and E-ALI-G when compared to C-G (p < 0.05). The IL-6, TNF-α, and CXCL2 mRNA expressions were higher in the animals that received LPS (ALI-G and E-ALI-G) compared to the C-G and E-G (p < 0.05). No statistically significant difference was observed in the BAL cellularity and in the expression of inflammatory mediators between the ALI-G and the E-ALI-G. The severity of ALI in response to intratracheal instillation of LPS did not show difference in rats with and without intratracheal-induced emphysema.
Subject(s)
Acute Lung Injury/chemically induced , Lipopolysaccharides , Pancreatic Elastase , Pulmonary Alveoli/pathology , Pulmonary Emphysema/chemically induced , Acute Lung Injury/genetics , Acute Lung Injury/metabolism , Acute Lung Injury/pathology , Animals , Bronchoalveolar Lavage Fluid/chemistry , Capillary Permeability , Chemokine CXCL2/genetics , Chemokine CXCL2/metabolism , Disease Models, Animal , Inflammation Mediators/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Macrophages, Alveolar/metabolism , Macrophages, Alveolar/pathology , Male , Neutrophil Infiltration , Pulmonary Alveoli/metabolism , Pulmonary Emphysema/genetics , Pulmonary Emphysema/metabolism , Pulmonary Emphysema/pathology , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats, Wistar , Severity of Illness Index , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism , Up-RegulationABSTRACT
Abnormalities in lungs caused by emphysema might alter their response to sepsis and the occurrence of acute lung injury (ALI). This study compared the extension of ALI in response to intraperitoneal lipopolysaccharide (LPS) injection in Wistar rats with and without emphysema induced by elastase. Adult male Wistar rats were randomized into four groups: control, emphysema without sepsis, normal lung with sepsis and emphysema with sepsis. Sepsis was induced, and 24 h later the rats were euthanised. The following analysis was performed: blood gas measurements, bronchoalveolar lavage (BAL), lung permeability and histology. Animals that received LPS showed significant increase in a lung injury scoring system, inflammatory cells in bronchoalveolar lavage (BAL) and IL-6, TNF-α and CXCL2 mRNA expression in lung tissue. Animals with emphysema and sepsis showed increased alveolocapillary membrane permeability, demonstrated by higher BAL/serum albumin ratio. In conclusion, the presence of emphysema induced by elastase increases the inflammatory response in the lungs to a systemic stimulus, represented in this model by the intraperitoneal injection of LPS.
