Meeting Abstracts
» Isolation and Identification of Factors Present within Pulmonary Edema Fluid which Increase Amiloride-insensitive Ion Transport in Fetal Distal Lung Epithelial Cells.

M.S.Harris, BScH 1,2, B.Rafii, BScH 2, D.Mahuran, PhD 1,2, G.Otulakowski, PhD 1,2, N.Sweezey, MD 1,2, and H.O'Brodovich, MD 1,2. 1University of Toronto, Toronto, ON, Canada and 1 Hospital for Sick Children, Toronto, ON, Canada.

The clearance of alveolar pulmonary edema occurs by active transepithelial ion transport, half of which is amiloride-insensitive. In primary cultures of rat fetal distal lung epithelium (FDLE), amiloride-insensitive short circuit current (Isc) is more than doubled by pretreatment with cardiogenic pulmonary edema fluid (EF), which is derived from plasma (J Physiol. London 544:537-48, 2002). This increase in amiloride-insensitive Isc in FDLE is abrogated if the EF is heat treated or completely digested by trypsin, suggesting that it is mediated by a protein, or a protein-dependent factor. When EF proteins were separated using Cibacron Blue dye affinity chromatography, the activity of EF that stimulated amiloride-insensitive Isc co-purified with albumin. Commercially available rat albumin (96% pure, Sigma) isolated from plasma also doubled amiloride-insensitive Isc in FDLE. This activity was removed from albumin or EF by incubation with activated charcoal for 48 hours. In conclusion, factors associated with albumin within cardiogenic EF induce amiloride-insensitive Isc in FDLE. Identification and isolation of the active factor(s) within the EF may provide a novel therapy for pulmonary edema.

Funded by: The Heart and Stroke Foundation of Ontario

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