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Mechanisms controlling the volume of pleural fluid and extravascular lung water

G. Miserocchi
European Respiratory Review 2009 18: 244-252; DOI: 10.1183/09059180.00002709
G. Miserocchi
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  • FIGURE 1.
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    FIGURE 1.

    a) At functional residual capacity, lung and chest walls exert on each other a recoil pressure equal in module but opposite in sign. Mechanical coupling is assured by pleural liquid pressure (Pliq) that is more negative than the recoil pressure of the structures. As a consequence, the visceral and parietal pleura push one against the other (as suggested by the solid deformed body). b) Actual touching between opposing pleurae does not occur because of repulsive forces between several layers of phospholipids adsorbed on mesothelial surfaces carrying charges of the same sign.

  • FIGURE 2.
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    FIGURE 2.

    Simple schematic diagram of a lung septal region depicting the pressures acting on the unit. Also in this case interstitial pressure (Pi) is more negative than that generated by lung recoil pressure.

  • FIGURE 3.
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    FIGURE 3.

    Model of control of pleural fluid and lung interstitial fluid volume based on the balance between microvascular filtration and lymphatic absorption.

  • FIGURE 4.
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    FIGURE 4.

    Polarisation of filtration/drainage processes in the pleural cavity and of intrapleural fluxes. White arrow: filtration; black arrow: lymphatic drainage; grey arrow: intrapleural fluxes.

  • FIGURE 5.
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    FIGURE 5.

    Sensitivity analysis describing the features of the lymphatic control on pleural liquid volume. Point A corresponds to the physiological condition. The ordinate shows that pleural liquid volume would only be slightly increased when microvascular filtration is increased 10 times (point B) or when the maximum lymphatic flow is decreased to 1:10 of normal (point C). Outside the chequered area (point D) no lymphatic control is operating.

  • FIGURE 6.
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    FIGURE 6.

    Pleural fluid/serum total protein ratio (TPR) (corresponding to Embedded Image) plotted versus protein reflection coefficient. The original data were taken from the two regressions presented in [20] referring to exudates and transudates. The figure intends to show that since TPR is a unique function of protein reflection coefficient, moving from transudates (·········) to exudates (–––) just corresponds to progressively increasing damage of the mesothelium.

  • FIGURE 7.
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    FIGURE 7.

    The continuous line shows the time course of lung interstitial pressure when interstitial oedema develops (○). Note the marked increase in interstitial pressure for a minor change in extravascular water reflecting the very low compliance of the lung interstitial matrix. The dotted line shows the change in interstitial pressure when severe oedema develops (grey arrow). The decrease in pressure reflects the loss of integrity of the macromolecular structure of the extracellular matrix due to fragmentation of proteoglycans, which results in an increase in tissue compliance and in microvascular permeability. Restoring the filtration gradient leads to unopposed filtration and severe oedema (arrow). •: control.

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Mechanisms controlling the volume of pleural fluid and extravascular lung water
G. Miserocchi
European Respiratory Review Dec 2009, 18 (114) 244-252; DOI: 10.1183/09059180.00002709

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Mechanisms controlling the volume of pleural fluid and extravascular lung water
G. Miserocchi
European Respiratory Review Dec 2009, 18 (114) 244-252; DOI: 10.1183/09059180.00002709
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  • Article
    • Abstract
    • INTERACTION BETWEEN LUNG MECHANICS AND EXTRAVASCULAR FLUID DYNAMICS
    • THE GENERAL MODEL FOR CONTROL OF EXTRAVASCULAR WATER
    • GENERAL CONCEPTS OF CONTROL
    • PLEURAL FLUID
    • LUNG INTERSTITIAL FLUID
    • CONCLUSION
    • Statement of interest
    • References
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