The pleura: the outer space of pulmonary medicine

In this issue of the Journal, MISEROCCHI [1] starts our series of articles on the pleura with a review of the physiology and the pathophysiology of the pleural space. In forthcoming months this series will cover a wide range of issues on pleural diseases. We have seen much progress in basic research as well as changing standards in the diagnosis and management of pleural disorders in recent years. The aim of this series is to supply the readership of the Journal with a concise and up-to-date overview on these developments, bringing some of the important information from the outer of research down to the earth of everyday clinical practice. The understanding of the physiology of the pleural space has come a long way since the pioneering work by scientists, such as STARLING [2, 3] at the end of the last century and VON NEERGARD [4] in the 1920s, who developed pressure control models of pleural fluid turnover. The relevant pressures were identified as the pleural liquid pressure (resulting from the expanding force of the thoracic cage versus the recoil force of the lung), the capillary and oncotic pressures in both the visceral and parietal membranes, and the oncotic pressure of the pleural fluid itself. The early models initially suggested a pressure-driven fluid flow from the parietal side across the pleural space to the visceral pleura and subsequently, into the pulmonary interstitium. Such models were derived from studies of animals with a thin visceral membrane, in which the blood supply originates from branches of the pulmonary arteries (with low capillary pressures). Later, it was found that in some other mammals, including man, the visceral pleura is considerably thicker and the blood supply is from the systemic circulation (with higher capillary pressures). This means that once the fluid enters the pleural space, there is no clear local pressure gradient to explain its further distribution. Thus, pressure models in man fall short in explaining the existence of a constant physiological amount of fluid in the pleural cavity and also, they do not give a clue as to the further fate of the fluid. In other words, volume control mechanisms need to be