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Am J Physiol Lung Cell Mol Physiol 280: L881-L887, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 5, L881-L887, May 2001

Pulmonary interstitial pressure and tissue matrix structure in acute hypoxia

Giuseppe Miserocchi1, Alberto Passi2, Daniela Negrini3, Massimo Del Fabbro3, and Giancarlo De Luca2

1 Department of Experimental and Environmental Medicine and Biotechnology, University of Milano-Bicocca, 20052 Monza; 3 Department of Medicine, Surgery and Dentistry, University of Milano, 20142 Milan; and 2 Department of Experimental and Clinical Biomedical Sciences, University of Insubria, 21100 Varese, Italy

Pulmonary interstitial pressure was measured via micropuncture in anesthetized rabbits in normoxia and after breathing 12% O2. In normoxia [arterial PO2 = 88 ± 2 (SD) mmHg], pulmonary arterial pressure and pulmonary interstitial pressure were 16 ± 8 and -9.6 ± 2 cmH2O, respectively. After 6 h of hypoxia (arterial PO2 = 39 ± 16 mmHg), the corresponding values were 30 ± 8 and 3.5 ± 2.5 cmH2O (P < 0.05). Pulmonary interstitial proteoglycan extractability, evaluated by hexuronate assay after 0.4 M guanidinium hydrochloride extraction, was 12.3, 32.4, and 60.6 µg/g wet tissue in normoxia and after 3 and 6 h of hypoxia, respectively, indicating a weakening of the noncovalent bonds linking proteoglycans to other extracellular matrix components. Gel filtration chromatography showed an increased fragmentation of chondroitin sulfate- and heparan sulfate-proteoglycans during hypoxic exposure, accounting for a loss of extracellular matrix native architecture and basement membrane structure. Gelatin zymography demonstrated increased amounts of the proteolytically activated form of gelatinase B (matrix metalloproteinase-9) after hypoxic exposure, providing evidence that the activation of proteinases may play a role in hypoxia-induced lung injury.

high-altitude pulmonary edema; micropuncture; microvascular permeability; proteoglycans; metalloproteinases


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