The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology
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Comparative Study
The effect of positive end-expiratory pressure on respiratory resistive properties in anaesthetized paralysed humans.
The respiratory resistive properties of the normal human respiratory system are volume-dependent. The overall flow resistance (Rmax,rs) can be partitioned into airway resistance (Raw) and the additional resistance (delta Rrs) which may result from the viscoelastic properties of the respiratory system, from inequality of time constants (pendelluft), or from both. Because positive end-expiratory pressure (PEEP) increases end-expiratory lung volume and may equalize ventilation within the lungs, the effect of PEEP on Raw, delta Rrs, and their sum (Rmax,rs) was assessed in anaesthetized surgical patients without evidence of lung disease. ⋯ We conclude that the overall flow resistance was not affected by PEEP. In contrast, PEEP clearly modified the contribution of its two components. The decrease in Raw with PEEP could have resulted, at least in part, from modification in the basal vagal tone.
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The phenotype of alveolar macrophages (AMs) is known to be modulated during pathological immune reactions in the lung. In this study, we wanted to determine the relationship between the AM phenotype and changes in the proportions of the various immune cells in bronchoalveolar lavage (BAL). BAL was performed in 76 consecutive patients, including 32 with sarcoidosis, 8 with idiopathic pulmonary fibrosis, 9 with pneumoconiosis, 13 with other respiratory disorders, and 14 controls without evidence of interstitial lung disease. ⋯ Eosinophils in BAL were not associated with a significant increase in AM membrane antigen expression. Prominent changes of the AM phenotype were found in active sarcoidosis showing lymphocytic alveolitis, with more frequent expression of CD54, KiM2, CD71, CD11b and RFD9. In conclusion, this study shows that the phenotype of AMs is related to the type and intensity of the immunopathological reaction in the lung, and correlates with the proportions of bronchoalveolar cells.
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We have previously shown that a decreased level of phosphatidylglycerol in cystic fibrosis (CF) respiratory mucus is partly responsible for its marked adhesiveness and stickiness, which impair mucus transport, and that distearoyl phosphatidylglycerol (DSPG) was the most efficient form of phosphatidylglycerol in the enhancement of respiratory mucus clearance. The aim of our study was to analyse the effect of distearoyl phosphatidylglycerol liposomes on the transport by cough and cilia of cystic fibrosis respiratory mucus. The surface and transport properties of mucus were measured: 1) on native cystic fibrosis mucus; 2) on cystic fibrosis mucus complemented with DSPG liposomes at a non-cytotoxic concentration; and 3) on cystic fibrosis mucus complemented with water. ⋯ For mucociliary transport, the cystic fibrosis mucus was transported at a higher rate with DSPG liposomes and water compared to native cystic fibrosis mucus. The cough clearance of cystic fibrosis respiratory mucus was significantly improved in the presence of DSPG and water, but the effect was more pronounced with DSPG liposomes than with water. We conclude that the use of DSPG liposomes as a lubricating agent proves to be an interesting therapeutic approach for improving the cough and mucociliary transport in cystic fibrosis patients.
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The time-course of volume change during passive expiration preceded by an end-inspiratory hold was studied with a biexponential model in six adult respiratory distress syndrome (ARDS) patients. We measured the initial volumes and time constants of the fast (tau 1), and the slow (tau 2) compartments of expiration, as well as the static elastance of the respiratory system. ⋯ We observed that: 1) the biexponential model fitted closely the volume decay; 2) the fast compartment was responsible for 81 +/- 7% (ARDS) versus 84 +/- 10% (controls) of the total volume exhaled, with tau 1 = 0.35 +/- 0.11 s (ARDS) versus 0.50 +/- 0.22 s (controls); 3) the slow compartment contributed only 19 +/- 6% (ARDS) versus 16 +/- 7% (controls), with tau 2 = 4.67 +/- 2.38 s (ARDS) versus 3.27 +/- 1.54 s (controls); and 4) static elastance was higher in ARDS patients. The findings could be explained in terms of a four parameter viscoelastic model of the respiratory system.