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

Abstract

The dose dependence and time course of smoke inhalation injury were determined in a rabbit model. Animals were insufflated with 18-90 breaths of cotton smoke or room air (control) at a rate of 18 breaths/min and tidal volume of 12 ml/kg. Smoke-exposed animals exhibited dose-related histologic effects with progressive deterioration of respiratory function during the postexposure period of observation (96 h). The smoke-exposed rabbits had reproducible injuries to both airway mucosa and lung parenchyma, manifested by disruption and sloughing of airway and alveolar epithelia, and exudation of protein-rich fluid and leukocytes into the airway and alveolar spaces. Significant effects were evident by 24 h postexposure. Smoke inhalation also affected the respiratory burst of alveolar macrophages. Generation of superoxide anions by alveolar macrophages at 48 h postexposure was increased significantly after smoke inhalation (54 breaths). The present rabbit model should be useful for studying the interactions between pulmonary epithelial cells and leukocytes after smoke inhalation and for determining the role that abnormal functioning of alveolar macrophages plays in the development of smoke inhalation injury.

Development of an in vivo model of laryngeal burn injury

“…In the current study, unbleached cotton was employed to determine if smoke altered injury compared to heated air alone. Unbleached cotton was selected to avoid chemical injury that might occur from toxic smoke, as in other smoke inhalation studies . Heavy metals or other toxins can further alter local tissue responses, and this toxic exposure would likely alter the healing outcomes in our model.…”

Substance P antagonist CP-96345 blocks lung vascular leakage and inflammation more effectively than its stereoisomer CP-96344 in a mouse model of smoke inhalation and burn injury

“…Previous reports from this and other laboratories have indicated that toxic smoke causes progressive injury to the airways, followed by injury to lung parenchyma (Barrow et al 1990; Traber and Herndon 1991; Bidani et al 1999; Dost 1991). Even though rapid release of chemical mediators in the airways has been suggested as a mechanism for injury, there is limited understanding of the underlying processes…”

Mechanisms of toxic smoke inhalation and burn injury: Role of neutral endopeptidase and vascular leakage in mice

“…Previous reports from this and other laboratories have indicated that toxic smoke causes progressive injury to the airways, followed by injury to lung parenchyma (Barrow et al 1990; Traber and Herndon 1991; Bidani et al 1999; Dost 1991). Even though rapid release of chemical mediators in the airways is a suggested mechanism for injury, there is limited understanding of the underlying processes that lead to delayed parenchymal injury.…”