Abstract
The air blood barrier is a gas exchanger and is well designed to fulfill this task as its main feature is its minimum thickness that in turn reflects a minimum amount of extravascular water. The maintenance of a minimum water volume is due to mechanisms able to control interstitial fluid turnover and to offset transient conditions of increase in this volume. The hydraulic pressure in the lung interstitium is ~ -10 cmH2O and reflects the equilibrium between the lymphatic absorption pressure and the microvascular filtration through the basement membrane whose hydraulic permeability is kept very low due to the macromolecular organization of heparansulphate proteoglycans (HS-PGs). When microvascular filtration is increased, the increase in extravascular water is minimal in face of a considerable increase in interstitial pressure (up to ~ 5 cmH2O) because of the high elastance of the extracellular matrix thanks to the mechanical role of matrix chondroitin sulphate proteoglycans (CS-PGs). This increase in pressure buffers microvascular filtration. Hypoxia causes fragmentation of CS-PGs of the extracellular matrix and of HS-PGs of the basement membrane: the result is a decrease in tissue elastance and an increase in permeability of the endothelial and epithelial barriers. When the overall PGs fragmentation overcomes a critical threshold, severe lung edema develops. Recovery from severe lung edema requires that extracellular integrity is restored. We provide evidence for a prompt lung cellular response to interstitial edema. We interpret this response as a fine mechanism to detect minor increases in extravascular water and to promote the reparative process.
Key Words
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Botto L, Beretta E, Daffara R, Miserocchi G, Palestini P. Biochemical and morphological changes in endothelial cells in response to hypoxic interstitial edema. Respir Res10.1186/1 1465-9921-7-7, 2006.
Conforti E, Fenoglio C, Bernocchi G, Bruschi O, Miserocchi G. Morpho-functional analysis of lung tissue in mild interstitial edema. Am J Physiol(Lung Cell Mol Physiol) 282:L766-L774, 2002.
Crouch EC, Martin GR, BrodyJS, Laurie GW. Basement membrane. In: The Lung: Scientific Foundations, Ed. By R.G Crystal , J.B. West et al. Philadelphia, PA: Lippincott-Raven, vol.1, p. 769-791, 1997.
Daffara R, Botto L, Beretta E , Conforti E, Faini A, Palestini P, Miserocchi G. Endothelial cells as early sensors of pulmonary interstitial edema.J Appl Physiol97: 1575-1583, 2004.
Eggermont J, Trouet D, Carton I, Nilius B. Cellular function and control of volume –regulated anion channels. Cell Biochem Biophys35: 263-274, 2001.
Foster LJ, de Hoog CL, Mann M. Unbiased quantitative proteomics of lipid rafts reveals high specificity for signaling factors PNAS 2003 100: 5813-5818; published online before print April 30 2003, 10.1073/pnas.0631608100.
Grimbert FA, Martin D, Parker JC, Taylor AE. Lymph flow during increases in pulmonary blood flow and microvascular pressure in dogs. Am J Physiol (Heart Circ Physiol255 (24): H1149-H1155, 1988.
Hansen J, Olsen N, Feldt-Rasmussen B, Kanstrup L, Dechaux M, Dubray C, Richalet J. Albuminuria and overall capillary permeability of albumin in acute altitude hypoxia. J Appl Physiol,76: 1922-1927, 1994.
Hardingham T, Fosang AJ. Proteoglycans: many forms and many functions. FASEB J 6: 861-870, 1992.
Hascall V, Hascall G. Proteoglycans. In: Cell biology of extracellular matrix, Hay ED, ed. Plenum Press, New York, p. 39-63, 1981.
Herren B, Levkau B, Raines EW, Ross R. Cleavage of beta-catenin and plakoglobin and shedding of VE-cadherin during endothelial apoptosis: evidence for a role for caspases and metalloproteinases. Mol Biol Cel,9(6):1589-601, 1998.
Ingber DE. Tensegrity II. How structural networks influence cellular information processing networks. J Cell Science116: 1397-1408, 2003.
Mansfield KD, Simon MC, and Keith B. Hypoxic reduction in cellular glutathione levels requires mitochondrial reactive oxygen species (mtROS).J Appl Physiol 97:1358-1366, 2004.
Miserocchi G, Haxhiu Poskurica B , Del Fabbro M, Crisafulli B. Pulmonary interstitial pressure in premature rabbits. Respir Physiol102: 239-249, 1995.
Miserocchi G, Haxhiu Poskurica B and Del Fabbro M. Pulmonary interstitial pressure in anesthetized paralyzed newborn rabbits. J Appl Physiol77(5): 2260-2268, 1994.
Miserocchi G, Passi A, Negrini D, Del Fabbro M, De Luca G. Pulmonary interstitial pressure and tissue matrix structure in acute hypoxia. Am J Physiol (Lung Cell Mol Physiol)280: L881-L887, 2001.
Miserocchi G, Negrini D, Gonano C. Direct measurements of interstitial pulmonary pressure in in-situ lung with intact pleural space. J Appl Physiol69: 2168-2174, 1990.
Miserocchi G, Negrini D, Del Fabbro M, Venturoli D. Pulmonary interstitial pressure in intact in situ lung: the transition to interstitial edema. J Appl Physiol74: 1171-1177, 1993.
Miserocchi,G, Negrini D, Mukenge S, Turconi P, Del Fabbro M. Liquid drainage through the peritoneal diaphragmatic surface. J Appl Physiol66(4):1579-1585, 1989.
Miserocchi G, Negrini D, Passi A, De Luca G. Development of lung edema: interstitial fluid dynamics and molecular structure. News Physiol Sci16:66-71, 2001.
Mongin AA, Orlov SN. Mechanisms of cell volume regulation and possible nature of the cell volume sensor. Pathophysiology8(2):77-88, 2001.
Negrini D. Pulmonary microvascular pressure profile during development of hydrostatic edema. Microcirculation2: 173-180, 1995.
Palestini P, Calvi C, Conforti E, Botto L, Fenoglio C, and Miserocchi G. Composition, biophysical properties and morphometry of plasma membranes in pulmonary interstitial edema. Am J Physiol Lung Cell Mol Physiol282: L1382-L1390, 2002.
Parker R, Granger D, Taylor AE. Estimates of isogravimetric capillary pressures during alveolar hypoxia. Am J Physiol(Heart Circ Physiol)241(10): H732-H739, 1981.
Roberts CR, Weight TN, Hascall and VC. Proteoglycans. In: The Lung: Scientific Foundations, Ed. By RG Crystal , JB West et al. Philadelphia, PA: Lippincott-Raven, vol.1, p. 757-767, 1997.
Sabbadini M, Barisani D, Conforti E, Marozzi A, Ginelli E, Miserocchi G, Meneveri R. Gene expression analysis in interstitial lung edema induced by saline infusion. Bioch Bioph Acta-Mol Basis of Dis1638: 149-156, 2003.
Schoene R, Hackett P, Henderson W, Sage E, Chow M, Roach R, Mills W, Martin T. High-altitude pulmonary edema. Characteristics of lung lavage fluid. J Am Med Assoc256: 63-69, 1986.
Semenza Gl. HIF-1: mediator of physiological and pathophysiological responses to hypoxia. J Appl Physiol881474-80, 2000.
Taylor AE, Granger DN. Exchange of macromolecules across the microcirculation. In: Handbook of Physiology. The Cardiovascular System. Microcirculation.Bethesda, MD: Am. Physiol. Soc., sect.2, vol. IV, pt.1, chapt. 11, p.467-520, 1984.
Venturoli D, Crisafulli B, Del Fabbro M, Negrini D, Miserocchi G. Estimation of in vivo pulmonary microvascular interstitial geometry using digital image analysis. Microcirc1: 27-40, 1995.
Wagner W, Latham L, Kapen R. Capillary recruitment during airway hypoxia: role of pulmonary artery pressure. J Appl Physiol47: 383-387, 1979.
West J, Tsukimoto K, Mathieu-Costello O, Prediletto R. Stress failure in pulmonary capillaries. J Appl Physiol70: 1731-1742, 1991.
Yurchenko PD, Schnittny JC. Molecular architecture of basement membrane. FASEB J 4: 1577-1590, 1990.
Zoeller RA, Grazia TJ, La Camera P, Park J, Gaposchkin DP, and Farber HW. Increasing plasmalogen levels protects human endothelial cells during hypoxia. Am J Physiol (Heart Cir Physiol)283: H671-H679, 2002.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2007 Springer Science+Business Media, LLC
About this paper
Cite this paper
Miserocchi, G. (2007). Lung Interstitial Pressure and Structure in Acute Hypoxia. In: Roach, R.C., Wagner, P.D., Hackett, P.H. (eds) Hypoxia and the Circulation. Advances in Experimental Medicine and Biology, vol 618. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-75434-5_11
Download citation
DOI: https://doi.org/10.1007/978-0-387-75434-5_11
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-387-75433-8
Online ISBN: 978-0-387-75434-5
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)