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J. Biol. Chem., Vol. 281, Issue 29, 19892-19898, July 21, 2006

This Article Full Text Full Text (PDF) All Versions of this Article: 281/29/19892    most recent M602064200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Litvan, J. Articles by Ridge, K. M. Search for Related Content PubMed PubMed Citation Articles by Litvan, J. Articles by Ridge, K. M. Social Bookmarking                      What's this?

-Adrenergic Receptor Stimulation and Adenoviral Overexpression of Superoxide Dismutase Prevent the Hypoxia-mediated Decrease in Na,K-ATPase and Alveolar Fluid Reabsorption^*

Juan Litvan, Arturo Briva, Mindy S. Wilson, G. R. Scott Budinger, Jacob Iasha Sznajder, and Karen M. Ridge¹

From the Division of Pulmonary and Critical Care Medicine, Northwestern University Medical School and Medical Service, Veterans Affairs-Chicago Health Care System, Chicago, Illinois 60611

Hypoxia has been shown to cause lung edema and impair lung edema clearance. In the present study, we exposed isolated rat lungs to pO₂ = 40 mm Hg for 60 min or rats to 8% O₂ for up to 24 h and then measured changes in alveolar fluid reabsorption (AFR) and Na,K-ATPase function. Low levels of oxygen severely impaired AFR in both ex vivo and in vivo models. The decrease in AFR was associated with a decrease in Na,K-ATPase activity and protein abundance in the basolateral membranes from peripheral lung tissue of hypoxic rats. -Adrenergic agonists restored AFR in rats exposed to 8% O₂ (from 0.02 ± 0.07 ml/h to 0.59 ± 0.03 ml/h), which was associated with parallel increases in Na,K-ATPase protein abundance in the basolateral membrane. Hypoxia is associated with increased production of reactive oxygen species. Therefore, we examined whether overexpression of SOD2, manganese superoxide dismutase, would prevent the hypoxia-mediated decrease in AFR. Spontaneously breathing rats were infected with a replication-deficient human type 5 adenovirus containing cDNA for SOD2. An otherwise identical virus that contained no cDNA was used as a control (Adnull). Hypoxic Adnull rats had decreased rates of AFR (0.12 ± 0.1 ml/h) as compared with hypoxic AdSOD2 and normoxic control rats (0.47 ± 0.04 ml/h and 0.49 ± 0.02 ml/h, respectively), with parallel changes in Na,K-ATPase.

Received for publication, March 3, 2006 , and in revised form, April 20, 2006.

^* This work was supported by Grants PO1-HL71643, RO1-HL079190, and RO1-HL48129 from the National Institutes of Health and by the Department of Veteran Affairs (VA-MREP). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Northwestern University Medical School, Pulmonary and Critical Care Medicine, 240 E. Huron, McGaw M328, Chicago, IL 60611. Tel.: 312-503-1648; Fax: 312-908-4650; E-mail: kridge{at}northwestern.edu.

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