TY - JOUR T1 - Physiology and pathophysiology of pleural fluid turnover JF - European Respiratory Journal JO - Eur Respir J SP - 219 LP - 225 DO - 10.1183/09031936.97.10010219 VL - 10 IS - 1 AU - G Miserocchi Y1 - 1997/01/01 UR - http://erj.ersjournals.com/content/10/1/219.abstract N2 - The pleural space contains a tiny amount (approximately 0.3 mL.kg-1) of hypooncotic fluid (approximately 1 g.dL-1 protein). Pleural fluid turnover is estimated to be approximately 0.15 mL.kg-1.h-1. Pleural fluid is produced at parietal pleural level, mainly in the less dependent regions of the cavity. Reabsorption is accomplished by parietal pleural lymphatics in the most dependent part of the cavity, on the diaphragmatic surface and in the mediastinal regions. The flow rate in pleural lymphatics can increase in response to an increase in pleural fluid filtration, acting as a negative feedback mechanism to control pleural liquid volume. Such control is very efficient, as a 10 fold increase in filtration rate would only result in a 15% increase in pleural liquid volume. When filtration exceeds maximum pleural lymphatic flow, pleural effusion occurs: as an estimate, in man, maximum pleural lymph flow could attain 30 mL.h-1, equivalent to approximately 700 mL.day-1 (approximately 40% of overall lymph flow). Under physiological conditions, the lung interstitium and the pleural space behave as functionally independent compartments, due to the low water and solute permeability of the visceral pleura. Pleural fluid circulates in the pleural cavity and intrapleural fluid dynamics may be represented by a porous flow model. Lubrication between lung and chest wall is assured by oligolamellar surfactant molecules stratified on mesothelial cells of the opposing pleurae. These molecules carry a charge of similar sign and, therefore, repulse each other, assuring a graphite-like lubrication. ER -