Pulmonary responses to smoke inhalation: Morphologic changes in rabbits exposed to pine wood smoke

Dose Dependence and Time Course of Smoke Inhalation Injury in a Rabbit Model

“…Thus, the present rabbit model minics human lung pathology after smoke inhalation injury. The structural abnormalities observed in the present model, particularly the degree of parenchymal injury, are more extensive than those described in other rabbit models of smoke inhalation injury [12,17,24,26]. Previous investigators found that the injuries produced by exposure to wood smoke or diesel fuel-polycarbonate plastic smoke were confined primarily to the trachea, mainstem bronchi, and lobar bronchi of rabbits [12,24,26].…”

“…Rabbits are a large enough species to provide adequate numbers of alveolar macrophages for such studies. However, previous rabbit models of smoke inhalation injury [12,17,24,26] failed to exhibit damage to the lung parenchyma similar to the injuries observed in patients [5,14]. This difference may be related to differing levels of smoke exposure.…”

Second hand smoke and COPD: lessons from animal studies

“…In a study of rabbits exposed to pine wood smoke, Thorning and colleagues document reparative responses that include intact epithelial basal lamina acting as a substratum for proliferating reparative epithelial cells (Thorning et al, 1982). However, more recent studies have shown that as opposed to mice the smoke-exposed rabbit does not exhibit reversal of emphysematous changes after all-trans-retinoic acid treatment (Nishi et al, 2003).…”

Health effects assessment of exposure to particles from wood smoke

“…For example, exposure of laboratory animals to wood smoke effluents decreased ventilatory frequency and ventilatory response to CO 2 (Wong et al 1984), increased micro-vascular permeability and produced pulmonary oedema (Nieman et al 1989), caused necrotising tracheobronchial epithelial cell injury (Thorning et al 1982), possibly increased the lung cancer incidence in mice (Liang et al 1988), increased levels of angiotensin-1-converting enzyme in the lungs (BrizioMolteni et al 1984), and compromised pulmonary macrophage-mediated immune mechanisms important in anti-microbial defence (Zelikoff et al 1995a,b), most likely via alterations in the integrity of the macrophage surface membrane or cytoskeletal components (Fick et al 1984.…”