Expiratory and inspiratory chest computed tomography and pulmonary function tests in cigarette smokers. (1/118)

This study evaluated small airway dysfunction and emphysematous destruction of lung parenchyma in cigarette smokers, using chest expiratory high-resolution computed tomography (HRCT) and pulmonary function tests (PFT). The degree of emphysematous destruction was classified by visual scoring (VS) and the average HRCT number at full expiration/full inspiration (E/I ratio) calculated in 63 male smokers and 10 male nonsmokers (group A). The Brinkman smoking index (BI), defined as cigarettes x day(-1) x yrs, was estimated. Sixty-three smokers were divided into three groups by PFT: group B1 (n=7), with normal PFT; group B2 (n=21), with diffusing capacity of the lung for carbon monoxide (DL,CO) > or = 80% predicted, forced expiratory volume in one second (FEV1) < 80% pred and/or residual volume (RV) > 120% pred; and group B3 (n=35), with DL,CO < 80% pred, FEV1 < 80% pred and/or RV > 120% pred. Heavy smokers (BI > or = 600) (n=48) showed a significant increase in emphysema by both VS and E/I. E/I was significantly elevated in both group B2 (mean+/-SD 0.95+/-0.05) and B3 (0.96+/-0.06) compared with group B1 (0.89+/-0.03). VS could not differentiate group B2 (3.9+/-5.0) from B1 (1.1+/-1.6). These findings suggest that the expiration/inspiration ratio reflects hyperinflation and airway obstruction, regardless of the functional characteristics of emphysema, in cigarette smokers.  (+info)

Subcellular adaptation of the human diaphragm in chronic obstructive pulmonary disease. (2/118)

Pulmonary hyperinflation impairs the function of the diaphragm in patients with chronic obstructive pulmonary disease (COPD). However, it has been recently demonstrated that the muscle can counterbalance this deleterious effect, remodelling its structure (i.e. changing the proportion of different types of fibres). The aim of this study was to investigate whether the functional impairment present in COPD patients can be associated with structural subcellular changes of the diaphragm. Twenty individuals (60+/-9 yrs, 11 COPD patients and 9 subjects with normal spirometry) undergoing thoracotomy were included. Nutritional status and respiratory function were evaluated prior to surgery. Then, small samples of the costal diaphragm were obtained and processed for electron microscopy analysis. COPD patients showed a mean forced expiratory volume in one second (FEV1) of 60+/-9% predicted, a higher concentration of mitochondria (n(mit)) in their diaphragm than controls (0.62+/-0.16 versus 0.46+/-0.16 mitochondrial transections (mt) x microm(-2), p<0.05). On the other hand, subjects with air trapping (residual volume (RV)/total lung capacity (TLC) >37%) disclosed not only a higher n(mit) (0.63+/-0.17 versus 0.43+/-0.07 mt x microm(-2), p<0.05) but shorter sarcomeres (L(sar)) than subjects without this functional abnormality (2.08+/-0.16 to 2.27+/-0.15 microm, p<0.05). Glycogen stores were similar in COPD and controls. The severity of airways obstruction (i.e. FEV1) was associated with n(mit) (r=-0.555, p=0.01), while the amount of air trapping (i.e. RV/TLC) was found to correlate with both n(mit) (r=0.631, p=0.005) and L(sar) (r=-0.526, p<0.05). Finally, maximal inspiratory pressure (PI,max) inversely correlated with n(mit) (r=-0.547, p=0.01). In conclusion, impairment in lung function occurring in patients with chronic obstructive pulmonary disease is associated with subcellular changes in their diaphragm, namely a shortening in the length of sarcomeres and an increase in the concentration of mitochondria. These changes form a part of muscle remodelling, probably contributing to a better functional muscle behaviour.  (+info)

Long-term recovery of diaphragm strength in neuralgic amyotrophy. (3/118)

Diaphragm paralysis is a recognized complication of neuralgic amyotrophy that causes severe dyspnoea. Although recovery of strength in the arm muscles, when affected, is common, there are little data on recovery of diaphragm function. This study, therefore, re-assessed diaphragm strength in cases of bilateral diaphragm paralysis due to neuralgic amyotrophy that had previously been diagnosed at the authors institutions. Fourteen patients were recalled between 2 and 11 yrs after the original diagnosis. Respiratory muscle and diaphragm strength were measured by volitional manoeuvres as maximal inspiratory pressure and sniff transdiaphragmatic pressure. Cervical magnetic phrenic nerve stimulation was used to give a nonvolitional measure of diaphragm strength: twitch transdiaphragmatic pressure. Only two patients remained severely breathless. Ten of the 14 patients had evidence of some recovery of diaphragm strength, in seven cases to within 50% of the lower limit of normal. The rate of recovery was variable: one patient had some recovery after 2 yrs, and the rest took 3 yrs or more. In conclusion, in most patients with diaphragm paralysis due to neuralgic amyotrophy, some recovery of the diaphragm strength occurs, but the rate of recovery may be slow.  (+info)

Human lung volumes and the mechanisms that set them. (4/118)

Definitions of human lung volumes and the mechanisms that set them are reviewed in the context of pulmonary function testing, with attention to the distinction between functional residual capacity (FRC) and the static relaxation volume of the respiratory system, and to the circumstances in which FRC and residual volume are set by dynamic rather than by static mechanisms. Related terms, conventions, and issues are addressed, including some common semantic and conceptual difficulties, with attention to "gas trapping", "hyperinflation", and "restriction".  (+info)

Differential lung mechanics are genetically determined in inbred murine strains. (5/118)

Genetic determinants of lung structure and function have been demonstrated by differential phenotypes among inbred mice strains. For example, previous studies have reported phenotypic variation in baseline ventilatory measurements of standard inbred murine strains as well as segregant and nonsegregant offspring of C3H/HeJ (C3) and C57BL/6J (B6) progenitors. One purpose of the present study is to test the hypothesis that a genetic basis for differential baseline breathing pattern is due to variation in lung mechanical properties. Quasi-static pressure-volume curves were performed on standard and recombinant inbred strains to explore the interactive role of lung mechanics in determination of functional baseline ventilatory outcomes. At airway pressures between 0 and 30 cmH2O, lung volumes are significantly (P < 0.01) greater in C3 mice relative to the B6 and A/J strains. In addition, the B6C3F1/J offspring demonstrate lung mechanical properties significantly (P < 0.01) different from the C3 progenitor but not distinguishable from the B6 progenitor. With the use of recombinant inbred strains derived from C3 and B6 progenitors, cosegregation analysis between inspiratory timing and measurements of lung volume and compliance indicate that strain differences in baseline breathing pattern and pressure-volume relationships are not genetically associated. Although strain differences in lung volume and compliance between C3 and B6 mice are inheritable, this study supports a dissociation between differential inspiratory time at baseline, a trait linked to a putative genomic region on mouse chromosome 3, and differential lung mechanics among C3 and B6 progenitors and their progeny.  (+info)

Airway responsiveness to methacholine: effects of deep inhalations and airway inflammation. (6/118)

We determined the dose-response curves to inhaled methacholine (MCh) in 16 asthmatic and 8 healthy subjects with prohibition of deep inhalations (DIs) and with 5 DIs taken after each MCh dose. Flow was measured on partial expiratory flow-volume curves at an absolute lung volume (plethysmographically determined) equal to 25% of control forced vital capacity (FVC). Airway inflammation was assessed in asthmatic subjects by analysis of induced sputum. Even when DIs were prohibited, the dose of MCh causing a 50% decrease in forced partial flow at 25% of control FVC (PD(50)MCh) was lower in asthmatic than in healthy subjects (P < 0.0001). In healthy but not in asthmatic subjects, repeated DIs significantly decreased the maximum response to MCh [from 90 +/- 4 to 62 +/- 8 (SD) % of control, P < 0.001], increased PD(50)MCh (P < 0.005), without affecting the dose causing 50% of maximal response. In asthmatic subjects, neither PD(50)MCh when DIs were prohibited nor changes in PD(50)MCh induced by DIs were significantly correlated with inflammatory cell numbers or percentages in sputum. We conclude that 1) even when DIs are prohibited, the responsiveness to MCh is greater in asthmatic than in healthy subjects; 2) repeated DIs reduce airway responsiveness in healthy but not in asthmatic subjects; and 3) neither airway hyperresponsiveness nor the inability of DIs to relax constricted airways in asthmatic subjects is related to the presence of inflammatory cells in the airways.  (+info)

A novel non-invasive technique for measuring the residual lung volume by nitrogen washout with rapid thoracoabdominal compression in infants. (7/118)

BACKGROUND: The functional residual capacity (FRC), the only lung volume to be routinely measured in infants, is an unreliable volume landmark. In addition to FRC, the residual volume (RV) was measured by nitrogen washout using rapid thoracoabdominal compression (RTC) in nine infants with cystic fibrosis aged 5-31 months. METHODS: A commercial system for nitrogen washout to measure lung volumes and a custom made system to perform RTC were used. Lung volume was raised to an airway opening pressure of 30 cm H(2)O (V(30)). RTC was performed from V(30). The jacket pressure (Pj; 65-92 cm H(2)O) which generated the highest forced expiratory volume (mean 40.2 ml/kg; 95% confidence interval (CI) 33.03 to 47.33) was used during the RV manoeuvre. The infants were manually hyperventilated to inhibit the respiratory drive briefly. RTC was initiated during the last passive expiration. RV was estimated by measuring the volume of nitrogen expired after end forced expiratory switching of the inspired gas from room air to 100% oxygen while jacket inflation was maintained at the time of switching into oxygen during the post-expiratory pause. RESULTS: In each infant RV and FRC measurements were reproducible and did not overlap; the difference between mean values, which is the expiratory reserve volume, was statistically significant (p<0.05). Mean RV was 21.3 (95% CI 18.7 to 24.0), FRC was 25.5 (95% CI 22.8 to 28.1), and TLC(30) (total lung capacity at V(30)) was 61.5 (95% CI 54.4 to 68.7) ml/kg. These values were dependent on body length, weight and age. When measuring RV the period between switching to oxygen and the end of the Pj plateau was 0.301 (95% CI 0.211 to 0.391) s. The washout duration was longer for RV than for FRC measurement (80.9 s (95% CI 71.3 to 90.4) versus 72. 4 s (95% CI 64.9 to 79.8)) (p<0.001). CONCLUSIONS: A new non-invasive and reliable technique for routine measurement of RV in infants is presented.  (+info)

Density dependence of forced expiratory flows in healthy infants and toddlers. (8/118)

In older children and adults, density dependence (DD) of forced expiratory flow is present over the majority of the full flow-volume curve. In healthy subjects, DD occurs because the pressure drop from peripheral to central airways is primarily dependent on turbulence and convective acceleration rather than laminar resistance; however, an increase in peripheral resistance reduces DD. We measured DD of forced expiratory flow in 22 healthy infants to evaluate whether infants have low DD. Full forced expiratory maneuvers were obtained while the subjects breathed room air and then a mixture of 80% helium-20% oxygen. Flows at 50 and 75% of expired forced vital capacity (FVC) were measured, and the ratio of helium-oxygen to air flow was calculated (DD at 50 and 75% FVC). The mean (range) of DD at 50 and 75% FVC was 1.37 (1.22-1.54) and 1.23 (1.02-1.65), respectively, values similar to those reported in older children and adults. There were no significant relationships between DD and age. Our results suggest that infants, compared with older children and adults, have similar DD, a finding that suggests that infants do not have a greater ratio of peripheral-to-central airway resistance.  (+info)