Traditional thinking suggests that pleural fluid develops on the basis of systemic venous
hypertension or a primary pleural process. Recent investigations, however, indicate that both
acute lung injury and pulmonary venous
hypertension can be important in the pathogenesis of
pleural effusions. To evaluate the role of
acute lung injury in the formation of
pleural effusions, we developed a model of acute, reversible
lung injury in NZW rabbits. Intravenous
ethchlorvynol (ECV), known to produce permeability
edema in humans, was used to produce permeability
pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis.
Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar
hemorrhage (6 to 10 h), and
pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN
vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal
lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized
lung injury can result in
pleural effusions.