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Published ahead of print on August 18, 2005, doi:10.1164/rccm.200501-005OC
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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 1002-1007, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200501-005OC

Inhibition of Acid-induced Lung Injury by Hyperosmolar Sucrose in Rats

Zeenat Safdar, Maimiti Yiming, Gabriele Grunig and Jahar Bhattacharya

Lung Biology Laboratory, Division of Pulmonary-Critical Care Medicine, and Department of Pathology, College of Physicians and Surgeons, Columbia University, St. Luke's–Roosevelt Hospital Center, New York, New York

Correspondence and requests for reprints should be addressed to Jahar Bhattacharya, M.D., D.Phil., St. Luke's–Roosevelt Hospital Center, 1000 10th Avenue, New York, NY 10019. E-mail: jb39{at}columbia.edu

Rationale: Acid aspiration causes acute lung injury (ALI). Recently, we showed that a brief intravascular infusion of hyperosmolar sucrose, given concurrently with airway acid instillation, effectively blocks the ensuing ALI.

Objectives: The objective of the present study was to determine the extent to which intravascular infusion of hyperosmolar sucrose might protect against acid-induced ALI when given either before or after acid instillation.

Methods: Our studies were conducted in anesthetized rats and in isolated, blood-perfused rat lungs. We instilled HCl through the airway, and we quantified lung injury in terms of the extravascular lung water (EVLW) content, filtration coefficient (Kfc), and cell counts and protein concentration in the bronchoalveolar lavage. We infused hyperosmolar sucrose via the femoral vein.

Results: In anesthetized rats, airway HCl instillation induced ALI as indicated by a 52% increase of EVLW and a threefold increase in Kfc. However, a 15-min intravenous infusion of hyperosmolar sucrose given up to 1 h before or 30 min after acid instillation markedly blunted the increases in EVLW, as well as the increases in cell count, and in protein concentration in the bronchoalveolar lavage. Hyperosmolar pretreatment also blocked the acid-induced increase of Kfc. Studies in isolated perfused lungs indicated that the protective effect of hyperosmolar sucrose was leukocyte independent.

Conclusions: We conclude that a brief period of vascular hyperosmolarity protects against acid-induced ALI when the infusion is administered shortly before, or shortly after, acid instillation in the airway. The potential applicability of hyperosmolar sucrose in therapy for ALI requires consideration.

Key Words: acid aspiration syndrome • extravascular lung water • filtration coefficient • leukocyte count • lung blood content




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