A new experimental model of cigarette smoke-induced emphysema in Wistar rats

Abstract

OBJECTIVE:To describe a new murine model of cigarette smoke-induced emphysema.METHODS:Twenty-four male Wistar rats were divided into two groups: the cigarette smoke group, comprising 12 rats exposed to smoke from 12 commercial filter cigarettes three times a day (a total of 36 cigarettes per day) every day for 30 weeks; and the control group, comprising 12 rats exposed to room air three times a day every day for 30 weeks. Lung function was assessed by mechanical ventilation, and emphysema was morphometrically assessed by measurement of the mean linear intercept (Lm).RESULTS:The mean weight gain was significantly (approximately ten times) lower in the cigarette smoke group than in the control group. The Lm was 25.0% higher in the cigarette smoke group. There was a trend toward worsening of lung function parameters in the cigarette smoke group.CONCLUSIONS:The new murine model of cigarette smoke-induced emphysema and the methodology employed in the present study are effective and reproducible, representing a promising and economically viable option for use in studies investigating the pathophysiology of and therapeutic approaches to COPD.

Cell Therapy Decreases Inflammation and Improves the Morphology of the Lung Parenchyma in a Murine Model of Cigarette Smoke-Induced Emphysema

“…3). These results confirm that the animal model of emphysema -using an inhalation chamber developed by our group [15] -was effective in the induction of pulmonary emphysema in mice. Importantly, 21 days after cell infusion, there was no statistically significant difference between Lm values of mice treated with cells (BMMC or BMMSC) compared with those observed in the untreated group (UN) without emphysema, as presented in Fig.…”

“…One of the most used approaches to investigate possible therapies and treatments to human diseases consists on the use of animal models [10], and this is also the case for investigations of COPD. In the specific context of pulmonary disease investigation, exposure of laboratory animals to cigarette smoke has gained prominence in recent years, since it mimics the pathophysiological characteristics of the disease in humans [4], [11]- [15].…”

Effects of passive inhalation of cigarette smoke on structural and functional parameters in the respiratory system of guinea pigs

“…- 27 Such changes were pointed out by the study of Banerjee et al, 28 in which the guinea pigs that inhaled cigarette smoke exhibited inflammation and apoptosis, which leads to destruction of alveolar membranes and septal cells, causing pulmonary airspace enlargement, and such enlargement may have influenced the changes in pulmonary pressures in the present study. Page et al 29 add that, after exposure of airway sensory nerves to cigarette smoke, there is damage caused by cytotoxic mediators to the ciliary epithelium layer, increased mucus secretion, hyperresponsiveness, and vasodilatation, findings that are in agreement with those of the present study.…”

Effects of Modified Zhisou Powder on Airway Mucus Production in Chronic Obstructive Pulmonary Disease Model Rats with Cold‐Dryness Syndrome

“…For the parameters MV, PIF, PEF, Penh, and PAU, although significant decreases or increases occurred in both COPD and CDSCOPD rats when compared with normal rats, no difference was observed between COPD and CDSCOPD rats. We supposed that the reason might be attributed to the mild COPD symptoms in this study, which were due to the low amount of cigarettes used to produce cigarette smoke (only two pieces per day) when compared with previous study [23] or due to the rats as animals relatively resistant to development of COPD [24]. Therefore, intratracheal drip of elastase, an enzyme inducing emphysema phenotype, was used to promote the model establishment [25].…”