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Am J Physiol Lung Cell Mol Physiol 296: L140-L144, 2009. First published November 7, 2008; doi:10.1152/ajplung.90339.2008
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Impact of buffering hypercapnic acidosis on cell wounding in ventilator-injured rat lungs

Sean M. Caples,1 Deborah L. Rasmussen,1 Won Y. Lee,1 Marla Z. Wolfert,1 and Rolf D. Hubmayr1,2

1Thoracic Diseases Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, and 2Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota

Submitted 10 June 2008 ; accepted in final form 31 October 2008

We measured the effects of raising perfusate pH on ventilator-induced cell wounding and repair in ex vivo mechanically ventilated hypercapnic rat lungs. Lungs were randomized to one of three perfusate groups: 1) unbuffered hypercapnic acidosis, 2) bicarbonate-buffered hypercapnia, or 3) tris-hydroxymethyl aminomethane (THAM)-buffered hypercapnia. The membrane-impermeant label propidium iodide was added to the perfusate either during or after injurious ventilation providing a means to subsequently identify transiently wounded and permanently wounded cells in optical sections of subpleural alveoli. Normalizing perfusate pH in hypercapnic preparations attenuated ventilator-induced cell injury, particularly in THAM-buffered preparations. This was observed despite greater amounts of edema and impaired lung mechanics compared with other treatment groups. Protective effects of buffering of hypercapnic acidosis on injury and repair were subsequently confirmed in a cell scratch model. We conclude that buffering of hypercapnic acidosis attenuates plasma cell injury induced by mechanical hyperinflation.

tris-hydroxymethyl aminomethane; mechanical hyperinflation


Address for reprint requests and other correspondence: S. M. Caples, Division of Pulmonary and Critical Care Medicine, 200 1st St. SW, Rochester, MN 55905 (e-mail: caples.sean{at}mayo.edu)




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D O'Toole, P Hassett, M Contreras, B D Higgins, S T W McKeown, D F McAuley, T O'Brien, and J G Laffey
Hypercapnic acidosis attenuates pulmonary epithelial wound repair by an NF-{kappa}B dependent mechanism
Thorax, November 1, 2009; 64(11): 976 - 982.
[Abstract] [Full Text] [PDF]


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