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Hypoxia 2009 Speakers
Giuseppe Miserocchi
Department of Experimental Medicine, Università di Milano-Bicocca, Via Cadore 48, Monza, Italy
Email: giuseppe.miserocchi@unimib.it
Talk Title: Lung interstitial pressure and structure in acute hypoxia
Session: Lung fluid movement in hypoxia
Abstract: Our group has extensively studied hypoxia induced lung edema in an experimental model in anesthetized rabbits. In physiological conditions the hydraulic pressure in the lung interstitium is ~ -10 cm H2O and results from the matching between a powerful lymphatics drainage and a low endothelial microvascular permeability thanks to proteoglycans (PGs) of the basement membrane. Furthermore, the architectural design of the extracellular matrix (ECM) guarantees a strong resistance to edema due to low tissue compliance assured by large interfibrillar PGs organized within ECM through noncovalent bonds that appear strong enough to provide mechanical stability but also sufficiently weak to allow tissue movements. PGs are hydrophilic and thus can also control the amount of free water in the extracellular space. Due to the low tissue compliance, a negligible extravascular fluid accumulation (about 5-10%) results in a marked increase in interstitial pressure up to about 5 cm H2O that buffers further filtration. The lung normally displays a strong resistance to lung edema, reflecting a dynamic balance between synthesis and degradation of ECM components. Endothelial cells are likely involved in ECM turnover as they promptly modify their signaling apparatus acting as early sensors of edema. This balance is sharply turned towards degradation by hypoxia exposure that leads to progressive fragmentation of PGs of basement membrane due to activation of metalloproteases, causing an increase in microvascular permeability. Furthermore, fragmentation of interfibrillar substance PGs beyond a given threshold causes a sharp increase in tissue compliance and a drop of interstitial pressure towards zero: at this point unopposed filtration is restored leading to severe alveolar edema.

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