Increased microvascular and mesothelial permeability usually underlies the onset of most exudates. The mechanisms of increased microvascular permeability have been extensively studied, and the available knowledge has identified one of its key processes in cytoskeletal function 48; Advances in understanding its properties will result from the study of the modulation of the interaction of actomyosin by various inflammatory stimuli. The examination of the mechanisms of increased microvascular permeability is beyond the scope of this article: the reader is referred to the recent review by Michel and Curry 48. Microvascular permeability increases in two modalities: the opening of new spaces between cells, perhaps as a result of cell distancing, or the opening of transcellular signaling pathways, possibly by fusion of cytoplasmic vesicles with the cell membrane. In the first case, the „pore surface” increases without changing r, i.e. The permeability to water and small solutes is greater, but the leakage of macromolecules is still limited; In the second case, the permeability of macromolecules is also increased. A number of stimuli and mediators have been found to cause these effects in endothelium-48. The mesothelium may share some of the mechanisms, as some of the mediators known to be involved in impaired microvascular permeability are found in pleural exudates. The origin of these mediators may come either extrapleurally or from the pleural mesothelium itself, as activated mesothelial cells release a variety of chemokines, cytokines, and growth factors, all of which can affect permeability and become actively phagocytic, release oxidants and proteases, and express cell surface molecules (discussed in 23, 24, 106). This, in turn, affects the influx into the pleural space of a variety of inflammatory cells, which also produce mediators that promote changes in the mesothelian barrier. It is believed that cellular mechanisms, most likely differentiated according to the primary abnormality, are involved in the development of exudates associated with all forms of local inflammation (lung infection, embolism, pleurisy in systemic collagen diseases), and in malignant tumors, often associated with alteration of Jl due to direct damage to the pleural or mediastinal lymphatics. Exudates occur when the removal of proteins and cells from the pleural space is impaired, or when proteins (and cells) enter the pleural space through a leaky mesothelial membrane. Impaired lymphatic drainage can be a major cause of exudate.

In fact, a normal Jl,s, in addition to its contribution to fluid elimination, is crucial for maintaining a low πliq, as it helps remove proteins from the pleural space. As πliq increases, the pressure balance between pleurals is altered, favouring filtration and further hindering absorption. The effusion, often a transudate in its early stages 101, quickly becomes an exudate, even if there are no altered barrier permeability properties. Decreased lymphatic flow may result from direct involvement of the pleural lymphatic vessels, as in the case of pleural infiltration by infectious processes or malignancy 100–104 and blockage of the stoma by fibrin deposition in the later stages of parapneumonic effusions 104; or result from extrapleural lymphoid changes, such as hypoplasia of the lymphatic system, obstruction of the mediastinal lymphatics or chest duct 100–104. Increased systemic venous pressure may also reduce Jl by increasing the flow pressure in the thoracic canal 100–103. ΔP on the visceral pleura promotes fluid absorption 1, 2, 4, 6, 55, 56. The fluid was absorbed according to the starling forces of the pulmonary capillaries through the visceral pleura into the lungs of open-breasted and infused dogs 7, 74; Fluid absorption rates in dog lungs wrapped in impermeable membranes changed with fluid π, which corresponds to starling forces 75. With the above values of Pc (10 cmH2O), Pliq (−9 cmH2O), πc (29 cmH2O), πliq (∼3 cmH2O) and σ (∼0.9), the net absorption pressure through the parietal pleura during a respiratory cycle would be ∼4 cmH2O. If the Lp at such a ΔP were 0.7 μL·h−1·cm−2·cmH2O−1 7, the absorption rate (Jvisc) would be 0.18 mL·h−1·kg−1 (or 2.8 μL·h−1·cm−2 of the visceral pleura), an overestimation due to the probably overestimated Lp (see permeability characteristics).