A radiologic and microradiographic study of experimental pulmonary emphysema in dogs.

Abstract

Anumber of methods for producing pulmonary emphysema in laboratory animals have been studied (3, 4, 7, 9, 11, 18). Their value as models for human emphysema has been criticized mainly on the ground that they fail to simulate adequately the human form of the disease (18). This criticism is not entirely valid since human pulmonary emphysema probably has multiple etiologies leading to a large variety of pathologic, physiologic, and clinical manifestations (17). No animal model based upon a simple etiologic agent can compete in complexity with its human analog. The simple model, however, can provide insight into the mechanism for the production of specific pathophysiologic changes. This report is a study of a model for the disease based upon an inflammatory etiology described by Rossing (6, 19). He found that repeated subacute exposure of dogs to the pulmonary irritant gas phosgene produced a disease resembling human emphysema. Acute exposure to the gas resulted in pulmonary edema, but subacute exposure resulted in terminal bronchiolitis and alveolitis. After repeated exposure, the dogs developed an increased lower airway resistance and an abnormality of pulmonary gas mixing and at necropsy showed pathologic changes consistent with emphysema. This technic for producing an emphysema-like disease in dogs has been used to study gross radiologic changes and fine structural changes in the lungs. Methods Twenty adult beagles weighing between 6 and 11 kg were exposed weekly to a concentration of 0.8 mg/L of phosgene for thirty minutes. A continuous flow chamber with a volume of 280 L similar to the one described by Rossing was used (18). The animals were not anesthetized during exposure. Prior to the initial exposure of the series and one week after the final exposure of the series, a breath-by-breath nitrogen washout, inspiratory and expiratory chest roentgenography, and pulmonary wedge arteriography were performed. During the course of the exposures, chest films on nonanesthetized animals were obtained at frequent intervals to monitor the progression of the acute phase of the disease. For the initial and final studies, the dogs were anesthetized with 30 mg/kg Na pentobarbital. An endotracheal tube with a balloon cuff was inserted, and the animals were placed on a respiratory pump at a tidal volume of 250 to 300 ml and at a rate sufficient just to suppress normal respiration. The breath-by-breath nitrogen washout was done with a rapid nitrogen analyzer. End-breath nitrogen content was used to plot the washout curves (7, 19). The pump was stopped momentarily in full inspiration and expiration to obtain postero-anterior and lateral chest films for measurement of the thoracic index (4). This was defined as the anterior-posterior diameter/lateral diameter.