There are scarce reports on respiratory muscle strength in end-stage liver disease patients. On the other hand, decreased PaCO2 due to hyperventilation is well documented in patients with end-stage liver disease. Chronic dyspnoea is frequently reported by these patients, but it is not known if it is related to respiratory muscle strength and/or hyperventilation. We studied 48 consecutive, ambulatory, Caucasian patients (37 men) with end-stage liver disease, awaiting for liver transplantation. Chronic dyspnoea was rated according to the modified Medical Research Council (mMRC) 6-point scale. Routine lung function tests, maximum static expiratory (Pemax) and inspiratory (Pimax) mouth pressures were measured. Pattern of breathing (VE: minute ventilation; VT: tidal volume; RR: respiratory rate; VT/TI: mean inspiratory flow; TI/TTOT: duty cycle; TI: duration of inspiration) was also measured. Forty-three patients reported some degree of dyspnoea (mean±SD). mMRC was 2±1.1, Pemax%pred was 106±33 and Pimax%pred was 91±28. These pressures were found below the normal limits in 13 and 16 patients, respectively. Furthermore, mMRC was significantly correlated with Pemax and Pimax (r=-0.49, p<0.001; r=-0.41, p<0.01, respectively). VE (11.5±3.4, l), VT (0.770±0.311, l), RR (16±4, bpm) and VT/TI (0.46±0.13, l sec-1) were increased and PaCO2 (33±4, mmHg) was decreased, indicating hyperventilation. In contrast TI/TTOT (0.42±0.05) was normal. Statistically significant correlations were found for mMRC with TI and RR (r=-0.32, p=0.03; r=0.32, p=0.03; respectively). We conclude that in end-stage liver disease, there is an interrelationship between chronic dyspnoea, respiratory muscle strength, and hyperventilation.

Scarce reports exist on the symptom of dyspnoea in chronic renal failure patients. The aim of our study was to investigate the prevalence and severity of chronic dyspnoea in these patients and whether the severity of dyspnoea is different before and after hemodialysis. We recruited 25 patients with stage 5 (GFR<15ml/min) renal failure with (mean±SD) age = 52±11 years, hemodialysis duration = 5±4 years, urea = 141±26 mg/dl, creatinine = 10±2 mg/dl. None of the patients suffered from any concomitant pulmonary disease. We used the modified (m) MRC scale to assess chronic dyspnoea. Routine lung function tests in seated and supine positions position, closing volume (CV) with the single breath oxygen test, blood gases, Pimax, Pemax, P0.1, pattern of breathing were also measured. All of our patients (100%) complaint of some degree of dyspnoea before dialysis, which was significantly reduced after dialysis. The parameters that changed before and after dialysis were: Δ(m)MRC (-1±0.5, p<0.001), ΔWt% pred, (-3±1, p<0.001), ΔpH (0.1±0.05, p<0.001), ΔPimax%pred (33±8, p<0.001), ΔCC% predicted (-0.2±0.4, p= 0.032), and ΔP0.1 (-2±0.4, p<0.001) cm H2O. Backwards regression analysis showed that the only single factor changed significantly after dialysis and correlates with Δ(m)MRC is ΔP0.1 (r = 0.527, p=0.01). We conclude that hemodialysis improves dyspnoea by reducing central respiratory drive in patients with renal failure.

Introduction: Near the end of a maximal voluntary breath-hold, re-inhalation of the expired gas allows an additional period of breath-holding, indicating that the breaking point does not depend solely on chemical drive. We hypothesized that afferents from respiratory muscle and/or chest wall are significant in breath-holdingMethods: Nineteen normal adults breathed room air through a mouthpiece connected to a pneumotachograph and were instructed to breath-hold with and without voluntary regular respiratory efforts against an occluded airway.Results: Fifty one trials with and 53 without respiratory efforts were analyzed, The mean number of efforts per minute was 19 +/- 2.3 and the mean lowest airway pressure (P-aw) - 16.6 +/- 5.4 cmH(2)O. Breath-holding time (BHT) did not differ without (33.0 +/- 18.2 s) and with (29.3 +/- 12.3 s) efforts. In five patients arterial blood gasses were measured before and at the end of breath-holding and they did not differ between trials without and with efforts, indicating similar chemical drive. Our results suggest that afferents from respiratory muscle and/or chest wall are not the major determinants of BHT. (c) 2007 Elsevier B.V. All rights reserved.

The lung’s primary functions are to supply the blood with an adequate amount of oxygen and to remove carbon dioxide. These are achieved by the unique design of the lung, which ensures that air and blood are kept in intimate contact—though separate—to allow gas exchange, while maintaining its integrity in the face of the magnitude of insults that inevitably accompany a lifetime of exposure to ambient air and mechanical stress during cyclic breathing.

The term expiratory flow limitation (EFL) is used to indicate that maximal expiratory flow is achieved during tidal breathing and is characteristic of intrathoracic airflow obstruction. It should be noted that some experts use the term chronic airflow limitation as a synonym for chronic obstructive pulmonary disease (COPD) to indicate the reduction in maximum expiratory flow that occurs in this disease (and, indeed, in other pulmonary diseases); the latter term does not imply that expiratory flow limitation actually occurs during tidal breathing [1]–[3].

AIMS:We used for the first time a non-invasive optoelectronic plethysmography to assess breathing movements and to provide a quantitative description of chest wall kinematics during phonation.METHODS:Volumes of different chest wall compartments (abdomen and lung apposed to rib cage and abdomen) were assessed using optoelectronic plethysmography in 16 normal Italians (eight men) during reading, singing and high-effort whispering (HW).RESULTS:During phonation the breathing pattern was different from quiet breathing and exercise. (1) During phonation, tidal volume and expiratory time increased while inspiratory time decreased. The expiratory volume changes and flows during HW were considerably greater than during vocalization. During HW, the overall end-expiratory thoracic volume significantly decreased as a result of decreased volume of all compartments and essentially impinged on the maximal expiratory flow-volume curve. (2) While, as previously shown, during exercise the expired volume is due entirely to the abdomen, during phonation all three chest wall compartments contribute to it. Under all conditions studied breathing was, on average, more costal in females than in males but this was mainly related to different size rather than gender per se.CONCLUSIONS:Physical characteristics have a greater importance than gender in determining breathing pattern and chest wall kinematics during phonation. The activity of the control of expiration during phonation is more complex than during exercise.

Previous studies have shown that microsatellite (MS) DNA instability (MSI) is detectable in sputum cells in chronic obstructive pulmonary disease (COPD) and asthma. The aim of the present study was to investigate whether asthma and COPD could be distinguished at the MS DNA level.DNA was extracted from sputum cells and white blood cells from 63 COPD patients, 60 non-COPD smokers, 36 asthmatics and 30 healthy nonsmokers. Ten MS markers located on chromosomes 2p, 5q, 6p, 10q, 13q, 14q and 17q were analysed.No MSI was detected in non-COPD smokers or healthy nonsmokers. A significantly higher proportion of COPD patients exhibited MSI (49.2%) compared to asthmatics (22.2%). MSI was detected even in the mild stages of COPD (33.3%) and asthma (22.2%). No relationship was found between MSI and COPD severity. The most frequently affected marker was D14S588 (17.5% in COPD and 2.7% in asthma). The markers D6S344, G29802 and D13S71 showed alterations only in COPD, and G29802 was associated with a significantly decreased forced expiratory volume in one second FEV1 (% predicted), whereas MSI in D6S344 was associated with a significantly higher FEV1 (% pred).The frequency of microsatellite instability was higher in chronic obstructive pulmonary disease than in asthma, and microsatellite instability in three workers showed chronic obstructive pulmonary disease specificity. However, further studies are needed to verify the differences between chronic obstructive pulmonary disease and asthma at the microsatellite level.

Lung mechanics, exhaled NO (NOe), and TNF-alpha in serum and bronchoalveolar lavage fluid were assessed in eight closed and eight open chest, normal anesthetized rabbits undergoing prolonged (3-4 h) mechanical ventilation (MV) at low volume with physiological tidal volumes (10 ml/kg). Relative to initial MV on positive end-expiratory pressure (PEEP), MV at low volume increased lung quasi-static elastance (+267 and +281%), airway (+471 and +382%) and viscolelastic resistance (+480 and +294%), and decreased NOe (-42 and -25%) in closed and open chest rabbits, respectively. After restoration of PEEP, viscoelastic resistance returned to control, whereas airway resistance remained elevated (+120 and +31%) and NOe low (-25 and -20%) in both groups of rabbits. Elastance remained elevated (+23%) only in closed-chest animals, being associated with interstitial pulmonary edema, as reflected by increased lung wet-to-dry weight ratio with normal albumin concentration in bronchoalveolar lavage fluid. In contrast, in 16 additional closed- and open-chest rabbits, there were no changes of lung mechanics or NOe after prolonged MV on PEEP only. At the end of prolonged MV, TNF-alpha was practically undetectable in serum, whereas its concentration in bronchoalveolar lavage fluid was low and similar in animals subjected or not subjected to ventilation at low volume (62 vs. 43 pg/ml). These results indicate that mechanical injury of peripheral airways due to their cyclic opening and closing during ventilation at low volume results in changes in lung mechanics and reduction in NOe and that these alterations are not mediated by a proinflammatory process, since this is expressed by TNF-alpha levels.

Introduction. - To take in charge of an asthmatic child it is necessary to evaluate the lung function.Methods. - In this study, the Negative Expiratory Pressure (NEP) has been used for the first time in children with asthma. After lung spirometry by plethysmography, we have used the NEP to assess the prevalence of expiratory flow limitation (FL) during resting breath in 27 asthmatic children (mean age: 11 +/- 2,5 years) 3-4 days after a crisis in both sitting and supine positions.Results. - All the children presented an obstructive defect (FEV 1: 63 +/- 13% med) and a dynamic hyperinflation (FRC: 128 +/- 25% med). According to the NEP, 11 children presented an expiratory flow limitation (FL). Asthma was more severe in the FL than in non-FL children (GINA 2002 classification). Among the 11 FL children, 5 were FL in both sitting and supine position and 6 only in supine. Nine of the 27 children were FL with the conventional method. NEP seems a more accurate method to assess the clinical gravity of asthma than FEV 1. The reduction of FRC in the supine position probably explains the greater incidence of FL in supine position.Conclusion. - Because of its easy execution, NEP seems to be well adapted for children. Links between FL detected by NEP and clinical signs of asthma has to be assessed by furthers studies including more patients. (c) 2005 Elsevier SAS. Tous droits reserves.

Background: Surgical biopsy specimens have shown that T lymphocytes (TLs) infiltrate lung parenchyma in patients with idiopathic pulmonary fibrosis (IPF) and might play a pathogenetic role. BAIL, a far less invasive technique, has also been used for the investigation of IPF pathogenesis. However, controversy exists whether the BAL fluid cellular profile reflects the cellular composition of the lung parenchyma.Study objective: To compare infiltrating TLs subpopulations (CD4+, CD8+, and CD4+/CD8+ ratio) in lung tissue and BAL fluid.Patients and methods: Immunohistochemistry was performed according to the streptavidin-biotin method on the surgical biopsy specimens 4 12 untreated patients with IPF. The number of CD3+, CD4+, and CD8+ TLs was determined by observer-interactive computerized image analysis (SAMBA microscopic image processor; Meylan, France). In BAL fluid, the same TLs subpopulations were evaluated by flow cytometry.Results: In lung tissue, CD3+ TLs accounted for a mean (+/- SEM) of 28.8 +/- 7% of total cells, CD4+ TLs accounted for 14.5 +/- 4% of total cells (50.1 +/- 4% of CD3+ TLs), and CD8+ TLs accounted for 13.8 +/- 4% of total cells (47.4 +/- 4% of CD3+ TLs). In BAL fluid, lymphocytes accounted for 9.8 +/- 2.5% of total cells, CD4+ TLs accounted for 51.8 +/- 4% of CD3+ TLs, and CD8+ TLs accounted for 42.2 +/- 4% of CD3+ TLs. Tissue CD4+ and CD8+ TLs (expressed as a percentage of CD3+ TLs) correlated significantly with the number of CD4+ and CD8+ TLs in BAIL fluid (r = 0.846 and p = 0.001 vs; r = 0.692 and p = 0.013, respectively). A significant positive correlation was also found between the mean CD4+/CD8+ ratio found in tissue and BAL fluid (1.05 +/- 0.21 and 1.5 +/- 0.27, respectively; r = 0.832; p = 0.01).Conclusion: The results suggest that in patients with IPF, the TL subpopulations in BAL fluid reflect the pattern of lymphocytic infiltration in pulmonary parenchyma.