Bulletin europeen de physiopathologie respiratoire最新文献

Reference values for respiratory impedances in children are scarce and limited to the situation where pressure is varied at the mouth. Total respiratory impedance was therefore measured from 4 to 30 Hz in 69 healthy children (9-13 yr) with both a pressure input at the mouth (input impedance, Zin) and a pressure input at the chest (transfer impedance, Ztr). Zin was characterized by the average resistance (R), the low-frequency limit of resistance (R0), the slope of the resistance-frequency curve (S), respiratory elastance (E) and respiratory inertance (I). Similar coefficients (R0', S', E', I'), some of which however have slightly different physiological meanings, were derived from Ztr. R, R0 and R0' were found to be significantly correlated to body height (p less than 0.001) and, independently, to age (p less than 0.05): R (kPa X l-1 X s) = 1.76-5.29 10(-3) height (cm) -4.13 10(-2) age (yr). Elastances were better correlated to height than to age: E (kPa X l-1) = 20.95-0.101 height (cm) and inertances better correlated to age than to height: I (Pa X l-1 X s2) = 4.39-0.128 age (yr). S and S' were not correlated to biometric variables. No difference was found between children living in polluted (n = 36) and nonpolluted (n = 33) areas, except for S which was significantly lower in the first group (p less than 0.01).

The mechanisms whereby arterial carbon dioxide tension (PaCO2) remains constant despite varying rates of CO2 production are poorly understood. During the gynaecological operation of laparoscopy, the abdominal cavity is filled with CO2. An increase in the rate of CO2 delivery to the lung (less than 50%) occurs as a result of venous CO2 absorption. Respiratory control in 39 anaesthetized but spontaneously breathing women was studied during such exogenous CO2 loading. End-tidal CO2 tension (PACO2 - rapid infrared analyser) and minute-ventilation (Wright respirometer) were measured before and at 5 min intervals after peritoneal insufflation. Ventilation increased and mean PACO2 remained constant in these patients. Inhalational anaesthetics depress respiration and this was confirmed by raised control PACO2 values in this study. However, it appears that mechanisms underlying PACO2 homeostasis in the presence of a CO2 load are not depressed by inhalational anaesthetic in this study. These patients were probably hyperoxic. Peripheral arterial chemoreflexes are thought to be eliminated by hyperoxia. Therefore, it is likely that neural stimuli, from exploration of the abdomen, drove breathing. Furthermore, the fact that there was not a large fall in PACO2 may have been due to feedback via the central (brainstem) chemoreceptor.

We present new lung function reference values based on an investigation of 1024 healthy subjects aged 6-81 years. The dependent variables, i.e. VC, FEV1, RV, FRC, TLC, PEF, MEF50 and MEF25 are expressed as transcendent functions of age, body height and mass. A single equation covers the age range from 6 to 81 years and reflects certain phenomena such as growth, maturation, ageing, sex differences and the undermass-overmass effect. This allows a more accurate determination of individualized reference values and normal limits.

The gas exchange at rest and during exercise was measured in 50 healthy men, 25 lifelong nonsmokers and 25 smokers, between 20 and 65 years of age. Arterial blood samples were taken and expired air was collected at rest, supine and sitting, and during graded exercise. Prediction formulas for various gas exchange variables were obtained by multiple regression. Optimal conditions for gas transfer were present at light exercise. The arterial oxygen tension (PaO2) remained approximately constant during exercise, although in individual smokers and nonsmokers it decreased by up to 1.8 kPa (13.5 mmHg) between a workload of 50 W and the maximal workload. The lower limit for PaO2 at maximal exercise was about 10.7 kPa (80 mmHg). The alveolo-arterial difference in oxygen tension (PA-aO2) increased considerably with increased workload, from 1.09 +/- 1.05 kPa at 50 W to 3.1 +/- 0.9 kPa at maximal exercise. Ageing and tobacco smoking were associated with a decrease in PaO2 and an increase in PA-aO2 at rest in the supine position, but at maximal exercise neither PaO2 nor PA-aO2 was significantly influenced by age or tobacco smoking. In contrast, the dead space and total ventilation were increased during exercise by ageing and tobacco smoking.

The experiments were performed with thirteen anaesthetized rabbits breathing spontaneously through the larynx. Phrenic output was measured during tidal respiration in control conditions and in the course of progressive denervation of the laryngeal and tracheobronchial compartments. We have analysed changes in amplitude and the rate of rise of the integrated phrenic neurogram as well as the changes in TI, TE, TT and f of the respiratory timing after superior laryngeal nerves (SLN-s) section, section of the recurrent laryngeal nerves (RLN-s) and step-wise complete midcervical vagotomy. Nerve sections were performed by two methods: 1) bilateral SLN-s, RLN-s and cervical vagal neurotomy (horizontal method); 2) right-sided neurotomies of SLN, RLN and vagus followed by left-sided neurotomies of these nerves (vertical method). Laryngeal deafferentation did not greatly affect respiratory variables. Unilateral and especially bilateral vocal cord paralysis prolonged the respiratory cycle with enhanced TI/TT ratio, increased amplitude and rate of rise of the integrated phrenic neurogram. Maximum values of all parameters (the rate of rise excluded) were achieved after complete midcervical vagotomy. Of the two methods of denervation, the right-sided followed by left-sided denervation led to better adaptation of the organism to the respiratory disturbance (smaller changes in TI and TE compared with the control values). Denervation by the 'horizontal' method (paired section of the nerves) led to an abrupt failure of effective ventilation.

In four normal volunteers, differences between oesophageal pressure fluctuations (delta Pes) in the upper and lower parts of the oesophagus and mouth pressure fluctuations (delta Pm), simultaneously measured during panting against an occlusion, were evaluated. Averaged quasi static pressure-volume curves were obtained by measuring pressure in the upper and lower thirds of the oesophagus. The differences between delta Pes and delta Pm during panting, due to elastic recoil changes, were predicted from an exponential relationship fitted to the pressure-volume curves. The calculated errors were compared with those observed experimentally. In the lower part of the oesophagus, delta Pes was similar to delta Pm at lung volumes in the range of 50 to 70% of Vmax. Vmax was deduced from the asymptote of the exponential curve. Mean delta Pes/delta Pm was 0.98 +/- 0.08 (SD). In the upper oesophagus, delta Pes was lower than delta Pm. Mean delta Pes/delta Pm was 0.87 in the range of 50 up to 90% of Vmax with an SD +/- 0.15. At lung volumes above 90% of Vmax for the upper oesophagus and above 70% of Vmax for the lower oesophagus, the ratio of delta Pes to delta Pm exceeded 1 and progressively increased. The measured values were often higher than those predicted from the fitted curves, presumably due to a narrowed glottic aperture. We concluded that in normals both the positioning of the oesophageal balloon in the lower oesophagus and a lung volume near functional residual capacity (FRC) are prerequisites for the use of delta Pm as a control for delta Pes, or vice versa, during panting against an occlusion.

Dispersion of elastic properties within the lungs may contribute to the creation of a sloping alveolar plateau of the single-breath N2 washout curve. In this study we have systematically explored the behaviour of a simple two-compartment lung model with non-uniform pressure-volume characteristics. The inhomogeneity was expressed in terms of the ratio between the shape constants (k1/k2) of the compartmental pressure-volume curves and the ratio between compartmental RV/TLC (R-RV/TLC). The model simulations indicate that normal slope magnitudes can be achieved with a moderate degree of inhomogeneity (k1/k2 and R-RV/TLV = 2). The model simulations also show that a phase II-like shape of the curve--of non dead space origin--may occur and furthermore that single-breath TLC determinations increasingly underestimate true TLC as the R-RV/TLC deviates from unity. For a given degree of inhomogeneity, the model predicts the slope to increase with overall RV/TLC and k but decrease with TLC. The relations between these overall factors and the slope of phase III are also found in a patient group, where these factors explain approximately 61% of the slope variance.

Alveolar macrophages (AM) from control (n = 12) and atopic patients (n = 19, 12 without treatment, 4 treated with theophylline and 3 with theophylline and corticosteroid) were compared for their capacity to release mediators. AM were purified by 2 h adherence and challenged with either ubiquitous allergen, specific sensitizing allergens, anti-IgG or anti-IgE serum. The release of paf-acether, lyso paf-acether and beta-glucuronidase was measured. Paf-acether and its lyso derivative were assayed on washed rabbit platelets. Enzyme and mediator releases were obtained after specific allergenic or anti-IgE serum challenge of AM from untreated atopic patients. No release of paf-acether was detected from AM, from control or treated atopic patients after in vitro immunological challenge, whereas that of lyso paf-acether was greatly reduced in both treated groups. Release was obtained by immunological challenge of AM from control patients after passive sensitization with atopic serum. The release of mediators with bronchoconstriction activity by AM could represent an alternative causal pathway in human asthma.