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Physiology and pathophysiology of pleural fluid turnover
Full text linkTight 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 exudativ
Postinspiratory-ramp activity of diaphragm under inspiratory resistive load
No full textInspiratory ramp activity, postramp activity (PRA) of diaphragm and respiratory flow were studied in anesthetized rabbits and conscious humans under inspiratory resistive load. Under load with chloralose-urethane anesthesia neural inspiration lasted 124 +/- 12 msec more than under control conditions and end of mechanical inspiration lagged behind that of neural inspiration by 114 +/- 4 msec. With pentobarbital-urethane anesthesia corresponding changes under load were 67 +/- 18 msec and 44 +/- 6 msec; after SO2 block of slowly adapting stretch receptors in bronchi corresponding changes under load were nil and 65 +/- 7 msec. In humans corresponding changes under load were about 192 and 127 msec. Both in rabbits and humans time course of PRA under load was essentially unchanged. Hence, under load a considerable part of PRA (or all of it under pentobarbital-urethane anesthesia without SO2 block) occurred during inspiration and that occurring during expiration was smaller than under control conditions. Consequently, under load braking of expiratory flow was smaller and peak expiratory flow occurred earlier than under control conditions
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