Comparative permeability of canine visceral and parietal pleura

Payne, D. Keith; Kinasewitz, Gary T.; González, Esperanza

doi:10.1152/jappl.1988.65.6.2558

Cited by 49 publications

(51 citation statements)

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“…The Lp of the visceral pleuracapillary endothelium membrane obtained in situ (0.7- [7,74,75], is much lower than in stripped pleura [72,73], but may still be overestimated, because the mesothelium might also have been damaged in these experiments [7,74]. The Lp of the parietal pleura obtained in vivo (1.2 and 2.2 mL?h -1 ?cm -2 ?cmH 2 O -1 , in dogs and rabbits, respectively) [64] is y2 orders of magnitude lower than in stripped pleura [72,73], and slightly greater than Lp of microvascular endothelium [76,77]. The values, obtained by measurement of convective flows from the pleural space into a capsule glued to the parietal pleura (or to the endothoracic fascia in rabbits), may also be overestimated, because the large (-30 cmH 2 O) negative pressure applied to the unsupported interstitium may have stretched the pleura and enlarged the intercellular junctions [6,42].…”

Section: Permeability Characteristicsmentioning

confidence: 91%

“…Indeed, studies performed on pleura specimens stripped from the underlying tissues [72,73] provided extremely high values of permeability to water and solutes, which are now regarded as being due to the experimental conditions [28-30, 40-42, 55, 56, 64]. The Lp of the visceral pleuracapillary endothelium membrane obtained in situ (0.7- [7,74,75], is much lower than in stripped pleura [72,73], but may still be overestimated, because the mesothelium might also have been damaged in these experiments [7,74]. The Lp of the parietal pleura obtained in vivo (1.2 and 2.2 mL?h -1 ?cm -2 ?cmH 2 O -1 , in dogs and rabbits, respectively) [64] is y2 orders of magnitude lower than in stripped pleura [72,73], and slightly greater than Lp of microvascular endothelium [76,77].…”

Section: Permeability Characteristicsmentioning

confidence: 99%

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Physiology and pathophysiology of pleural fluid turnover

Zocchi¹

2002

Eur Respir J

171

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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...

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Section: Permeability Characteristicsmentioning

confidence: 91%

Section: Permeability Characteristicsmentioning

confidence: 99%

Physiology and pathophysiology of pleural fluid turnover

Zocchi¹

2002

Eur Respir J

171

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“…Results from studies on stripped specimens of the visceral pleura [33] suggest that permeability of the visceral pleura to water and solutes is fairly high. Contrary to these conclusions are the results from experiments where the integrity of the pleural space and spontaneous respiration were preserved; in these conditions, it was found that albumin transport from pleural space to pulmonary interstitium accounted for less than 20% (an overestimate) of total albumin removal from the pleural space with close to normal pleural liquid volume [23].…”

Section: Pleural Space and Lung Pathophysiologymentioning

confidence: 99%

Physiology and pathophysiology of pleural fluid turnover

Miserocchi¹

1997

Eur Respir J

240

126

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Number 1 in this SeriesA review on pleural space is certainly most welcome, for the simple reason that on opening a textbook of physiology the concepts concerning pleural fluid turnover date back to 1927 [1]. The same comment, in fact, applies in general to microvascular water and solute exchange. This appears particularly misleading, considering the major advances achieved in the field over the last 70 yrs. Around the turn of the 19th century, STARLING and TUBBY [2] interpreted microvascular fluid and solute exchange as resulting from the balance between hydraulic and colloidosmotic pressures. This concept is still valid today, but the complete formulation of transmicrovascular exchange has become much more complex because water crosses biological membranes more easily than large solutes (namely, plasma proteins) do [3]. In fact, different equations describe water and solute fluxes [4].As a result, the general model of transcapillary fluid exchange still taught to students, based on fluid filtration at the arteriolar end of the capillary bed and reabsorption at the venular end, appears rather simplistic. Due to the different permeability to water and solutes, one could predict on a mathematical basis that such a model would lead to a progressive increase in interstitial protein concentration over time [3,4], a condition that cannot be confirmed experimentally.Similarly, the old hypothesis claiming that pleural fluid filters at parietal level and is reabsorbed through the visceral pleura [1] would imply that pleural liquid protein concentration would keep increasing with age, but again there are no indications that this occurs. The existence of partial restriction to the movement of large solutes, compared to that of water molecules, posed scientists the major problem of explaining how interstitial volume and protein concentration are kept fairly steady. Ideologically, this led to re-evaluation of lymphatics as the major route for interstitial fluid drainage. In fact, since lymphatics do not sieve proteins, they leave the interstitial protein concentration unaltered the latter depending only upon the sieving properties of the filtering membrane. Accordingly, the description of interstitial fluid homeostasis under steady state conditions is now being explained as a balance between capillary filtration and lymphatic absorption. Major validation of this model has come from the accumulating experimental data over the past 30 yrs concerning interstitial tissues [4] and serous spaces [5]. Interestingly, since the pioneering, work of STARLING and TUBBY [2] the pleural space has been used as a useful experimental model to study the interaction between microvascular filtration and lymphatic drainage.This article presents an integrated view of pleural fluid turnover, based on data gathered from experimental studies on animals over the last 15 yrs. The situation in man is, unfortunately, still poorly defined; yet, where possible, Under physiological conditions, the lung interstitium and the pleural space behave as function...

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“…Μελέτες σε ιστούς τοιχωματικού [208,209] Η επιφάνεια του υπεζωκότα που φυσιολογικά αντικρύζει την υπεζωκοτική κοιλότητα θα αναφέρεται ως μεσοθηλιακή επιφάνεια ή πλευρική επιφάνεια (mesothelial), ενώ η επιφάνεια που αντικρύζει το διάμεσο ιστό (θωρακικό κλωβό ή πνεύμονα) θα αναφέρεται ως διάμεση επιφάνεια ή εξωπλευρική επιφάνεια (interstitial). Αντίστοιχα, η μεμβράνη που αντικρύζει την υπεζωκοτική κοιλότητα θα αναφέρεται ως κορυφαία μεμβράνη (basolateral membrane) ενώ η επιφάνεια που αντικρύζει το διάμεσο ιστό θα αναφέρεται ως βασική μεμβράνη (apical membrane).…”

Section: ο υ σ ι ε σ π ο υ χ ρ η σ ι μ ο π ο ι η θ η κ α ν σ τ η μ ε unclassified

Επιδράσεις Της Ινσουλίνης Και Των Ινσουλινοειδών Αυξητικών Παραγόντων (IGF) Στη Διακίνηση Του Υπεζωκοτικού Υγρού Στο Πρόβατο Και Στον Άνθρωπο

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Comparative permeability of canine visceral and parietal pleura

Cited by 49 publications

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Physiology and pathophysiology of pleural fluid turnover

Physiology and pathophysiology of pleural fluid turnover

Physiology and pathophysiology of pleural fluid turnover

Επιδράσεις Της Ινσουλίνης Και Των Ινσουλινοειδών Αυξητικών Παραγόντων (IGF) Στη Διακίνηση Του Υπεζωκοτικού Υγρού Στο Πρόβατο Και Στον Άνθρωπο

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