Pulmonary emphysema induced by passive smoking: an experimental study in rats

• Published in: Brazilian journal of medical and biological research Vol. 30; no. 10; pp. 1241 - 1247
• Main Authors: Cendon, S P, Battlehner, C, Lorenzi Filho, G, Dohlnikoff, M, Pereira, P M, Conceição, G M, Beppu, O S, Saldiva, P H
• Format: Journal Article
• Language: English
• Published: Brazil Associação Brasileira de Divulgação Científica 01-10-1997
• Subjects: Animals; BIOLOGY; emphysema; Male; MEDICINE, RESEARCH & EXPERIMENTAL; morphological analysis; passive smoking; Pulmonary Emphysema - etiology; pulmonary function; quantification; Rats; Rats, Wistar; Tobacco Smoke Pollution - adverse effects; pulmonary function; passive smoking; quantification; rats; emphysema; morphological analysis
• ISSN: 0100-879X; 1414-431X; 0100-879X; 1414-431X
• DOI: 10.1590/S0100-879X1997001000017

We describe a short time model for inducing experimental emphysema in rats by chronic tobacco smoke inhalation. Three groups of male Wistar rats (6 months old) were studied: controls (N = 8), rats intoxicated for 45 days (s-45, N = 7) or for 90 days (s-90, N = 8). The exposed animals were intoxicated 3 times a day (10 cigarettes per exposure period), 5 days a week. Pulmonary damage was assessed by means of functional tests and quantitative pathological examination of the airways and lung parenchyma. The s-45 and s-90 animals were similar in terms of functional residual capacity (FRC) corrected for body weight (FRC/kg) but both groups of smoking rats exhibited significantly higher FRC/kg values than the controls (s-45 = 6.33; s-90 = 6.46; controls = 3.78; P < 0.05). When the two groups of smoking rats were pooled together and compared to controls, they showed decreased lung elastance (1.6 vs 2.19; P = 0.046) and increased mean linear intercept (Lm) (85.14 vs 66.44; P = 0.025). The s-90 animals presented higher inflammation and muscular hypertrophy at the level of the axial bronchus than the controls (P < 0.05). When smoking groups were pooled and compared to controls, they presented significantly higher inflammation at the lateral level (P = 0.028), as well as airway secretory hyperplasia (P = 0.024) and smooth muscle hypertrophy (P = 0.005) at the axial level. Due to its simplicity, low cost and short duration, this technique may be a useful model to obtain new information about airspace remodeling due to chronic tobacco consumption.