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First published online July 18, 2008
Experimental Biology and Medicine 233:1202-1212 (2008)
doi: 10.3181/0801-RM-17
© 2008 by the Society for Experimental Biology and Medicine
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ORIGINAL RESEARCH ARTICLE

Pulmonary Histopathology in an Experimental Model of Chronic Aspiration Is Independent of Acidity

Tacy E. Downing*, Thomas A. Sporn{dagger}, R. Randal Bollinger*,{ddagger}, R. Duane Davis*, William Parker* and Shu S. Lin*,{ddagger},1

* Department of Surgery, {dagger} Department of Pathology, and {ddagger} Department of Immunology, Duke University, Durham, North Carolina 27710

To whom requests for reprints should be addressed at 1 Department of Surgery, Duke University Medical Center, DUMC Box 3392, Durham, NC 27710. E-mail: lin00003{at}mc.duke.edu

Gastroesophageal reflux has become a major health concern in industrialized countries, with drugs aimed at blocking acid production being more frequently prescribed than any other drug. Damage to lung tissue as a result of chronic aspiration of gastric fluid is a primary health risk associated with gastro-esophageal reflux, with such aspiration being suspected in the induction or exacerbation of asthma and other lung diseases. In this study, a rodent model of chronic aspiration was used to characterize the pulmonary histopathology produced by repetitive aspiration events and to investigate the pathologic roles of individual gastric fluid components such as acid and particulate food matter. Rats exposed to chronic aspiration of whole gastric fluid developed a pathology distinct from that of acute lung injury, characterized by granulomatous interstitial pneumonitis with prominent formation of multinucleated giant cells. This pattern of injury could be reproduced with chronic aspiration of particulate food matter and with chronic aspiration of pH-neutralized gastric fluid, but not with chronic aspiration of hydrochloric acid. Thus, since acid-neutralizing therapy is currently the mainstay of treatment for patients with reflux-associated respiratory symptoms, these results strongly suggest that alternative therapeutic approaches aimed at preventing chronic-aspiration induced lung injury may be warranted.

Key Words: chronic aspiration • gastroesophageal reflux disease, GERD • lung injury • pulmonary






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