Tight control of the volume and composition of the pleural liquid is necessary to ensure an efficient mechanical coupling between lung and chest wall. Liquid enters the pleural space through the parietal pleura down a net filtering pressure gradient. Liquid removal is provided by an absorptive pressure gradient through the visceral pleura, by lymphatic drainage through the stomas of the parietal pleura, and by cellular mechanisms. Indeed, contrary to what was believed in the past, pleural mesothelial cells are metabolically active, and possess the cellular features for active transport of solutes, including vesicular transport of protein. Furthermore, the mesothelium was shown, on the basis of recent experimental evidence, both in vivo and in vitro, to be a less permeable barrier than previously believed, being provided with permeability characteristics similar to those of the microvascular endothelium. Direct assessment of the relative contribution of the different mechanisms of pleural fluid removal is difficult, due to the difficulty in measuring the relevant parameters in the appropriate areas, and to the fragility of the mesothelium. The role of the visceral pleura in pleural fluid removal under physiological conditions is supported by a number of findings and considerations.Further evidence indicates that direct lymphatic drainage through the stomas of the parietal pleura is crucial in removing particles and cells, and important in removing protein from the pleural space, but should not be the main effector of fluid removal. Its importance, however, increases markedly in the presence of increased intrapleural liquid loads. Removal of protein and liquid by transcytosis, although likely on the basis of morphological findings and suggested by recent indirect experimental evidence, still needs to be directly proven to occur in the pleura. When pleural liquid volume increases, an imbalance occurs in the forces involved in turnover, which favours fluid removal. In case of a primary abnormality of one ore more of the mechanisms of pleural liquid turnover, a pleural effusion ensues. The factors responsible for pleural effusion may be subdivided into three main categories: those changing transpleural pressure balance, those impairing lymphatic drainage, and those producing increases in mesothelial and capillary endothelial permeability. Except in the first case, pleural fluid protein concentration increases above normal: this feature underlies the classification of pleural effusions into transudative and exudative. Eur Respir J 2002; 20: 1545-1558. The thin layer of liquid present between the pleural surfaces has the important function of providing the mechanical coupling between the chest wall and lung, which ensures instantaneous transmission of perpendicular forces between the two structures, and allows their sliding in response to shearing forces [1,2]. It also provides lubrication of the reciprocal motions of the two structures during breathing. Two views, in part compatible, exist on the nature of t...

In 11 mechanically ventilated patients, respiratory mechanics were measured 1) during constant flow inflation and 2) following end-inflation airway occlusion, as proposed in model analysis (J. Appl. Physiol. 58: 1840-1848, 1985. During the latter part of inflation, the relationship between driving pressure and lung volume change was linear, allowing determination of static respiratory elastance (Ers) and resistance (RT). The latter represents in each patient the maximum resistance value that can obtain with the prevailing time constant inhomogeneity. Following occlusion, Ers and RT were also obtained along with RT (min) which represents a minimum, i.e., resistance value that would obtain in the absence of time constant inhomogeneity. A discrepancy between inflation and occlusion Ers and RT was found only in the three patients without positive end-expiratory pressure, and could be attributed to recruitment of lung units during inflation. In all instances Ers and RT were higher than normal. RT(min) was lower in all patients than the corresponding values of RT, indicating that resistance was frequency dependent due to time constant inequalities. Changes in inflation rate did not affect Ers, while RT increased with increasing flow.

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Diffusional permeability (P) to sucrose (Psuc) and Na+ (PNa+) was determined in specimens of rabbit sternal parietal pericardium, which may be obtained without stripping. Specimens were mounted in an Ussing apparatus with 3H-labeled sucrose and 22Na+ in a luminal (L) or interstitial (I) chamber. Psuc was 2.16 +/- 0.44 for L-->I and 2.63 +/- 0.45 (SE) x 10(-5) cm/s for I-->L, i.e., approximately 10 times smaller than that previously obtained in stripped specimens of pleura despite the similarity of intercellular junctions in pericardium and pleural mesothelium of various species. These findings suggest that previous Psuc was overestimated because stripping damages the mesothelium. PNa+ (x10(-5) cm/s) was 7.07 +/- 0.71 for L-->I and 7.37 +/- 0.69 x 10(-5) cm/s for I-->L. Measurements were also done with phospholipids, which are adsorbed on the luminal side of mesothelium in vivo. With phospholipids in L, Psuc was 0.75 +/- 0.10 and 0.65 +/- 0.08 and PNa+ was 3.80 +/- 0.32 and 3.76 +/- 0.15 x 10(-5) cm/s for L-->I and I-->L, respectively, i. e., smaller than without phospholipids. With phospholipids in I (where they are not adsorbed), Psuc (2.33 +/- 0.42 x 10(-5) cm/s) and PNa+ (7.01 +/- 0.45 x 10(-5) cm/s) were similar to those values without phospholipids. Hence, adsorbed phospholipids decrease P of mesothelium. If the mesothelium were scraped away from the specimen, Psuc of the connective tissue would be 13.2 +/- 0.76 x 10(-5) cm/s. Psuc of the mesothelium, computed from Psuc of the unscraped and scraped specimens, corrected for the effect of unstirred layers (2. 54 and 19.4 x 10(-5) cm/s, respectively), was 2.92 and 0.74 x 10(-5) cm/s without and with phospholipids, respectively. Hence, most of the resistance to diffusion of the pericardium is provided by the mesothelium.