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1.
Flow limitation in a collapsible elastic tube is dependent on the area (A) vs. pressure (P) relationship (the "tube law") for the tube. In this paper, a tube law in which A varies as (1-P)-n1 at negative pressures is assumed. It is shown that wave-speed limitation is possible at negative pressures only if n1 is greater than 0.5. Dissipative limitation is also investigated. Viscous limitation can occur if n1 is greater than 0.5, and turbulent limitation can occur if n1 is not less than 0.4. For values of n1 less than 0.4, flow cannot be limited at negative pressures. Model simulations are used to show that a combination of a value of n1 less than 0.3 together with an area minimum in the bronchial tree produce a minimum (a "hook") in the flow-volume curve. In the vicinity of such hooks, density dependence exceeds the usually accepted theoretical maximum value. Simulations also show that, when n1 is sufficiently small, apparently supramaximal flows appear to be possible.  相似文献   

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Two groups of subjects were studied: one with (group 1: 5 healthy and 4 mildly asthmatic subjects) and another without (group 2:9 moderately and severely asthmatic subjects) a plateau of response to methacholine (MCh). We determined the effect of deep inhalation by comparing expiratory flows at 40% of forced vital capacity from maximal and partial flow-volume curves (MEF40M/P) and the quasi-static transpulmonary pressure-volume (Ptp-V) area. In group 1, MEF40M/P increased from 1.58 +/- 0.23 (SE) at baseline up to a maximum of 3.91 +/- 0.69 after MCh when forced expiratory volume in 1 s (FEV1) was decreased on plateau by 24 +/- 2%. The plateau of FEV1 was always paralleled by a plateau of MEF40M/P. In group 2, MEF40 M/P increased from 1.58 +/- 0.10 at baseline up to a maximum of 3.48 +/- 0.26 after MCh when FEV1 was decreased by 31 +/- 3% and then decreased to 2.42 +/- 0.24 when FEV1 was decreased by 46 +/- 2%. Ptp-V area was similar in the two groups at baseline yet was increased by 122 +/- 9% in group 2 and unchanged in group 1 at MCh end point. These findings suggest that the increased maximal response to MCh in asthmatic subjects is associated with an involvement of the lung periphery.  相似文献   

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Background  

Maximum pressures developed by the respiratory muscles can indicate the health of the respiratory system, help to determine maximum respiratory flow rates, and contribute to respiratory power development. Past measurements of maximum pressures have been found to be inadequate for inclusion in some exercise models involving respiration.  相似文献   

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The aim of the present study was to analyse the effect of 1 year of intensive swimming training on lung volumes, airway resistance and on the flow-volume relationship in prepubertal girls. Five girls [9.3 (0.5) years old] performing vigorous swimming training for 12 h a week were compared with a control group of 11 girls [9.3 (0.5) years old] who participated in various sport activities for 2 h per week. Static lung volumes, maximal expiratory flows (MEF) at 75, 50 and 25% of vital capacity, 1-s forced expiratory volume (FEV1.0) and airway resistance (R aw) were measured by means of conventional body plethysmograph techniques. Prior to the training period there were no significant differences between the two groups for any of the parameters studied. Moreover, for both groups, all parameters were within the normal range for children of the corresponding age. After 1 year of training, vital capacity (VC), total lung capacity (TLC) and functional residual capacity (FRC) were larger (P<0.05) in the girl swimmers than in the control group, while physical development in terms of height and weight was similar. FEV1.0 (P<0.01), MEF25, MEF50 (P<0.05) and MEF75 as well as the ratio MEF50 / TLC (P<0.05) had increased in the girl swimmers but were unchanged in the control group. R aw tended to be lower in the girl swimmers and higher in the control group. The results indicate that intensive swimming training prepuberty enhances static and dynamic lung volumes and improves the conductive properties of both the large and the small airways. As to the causative mechanism, it can be speculated that at prepuberty intensive swimming training promotes isotropic lung growth by harmonizing the development of the airways and of alveolar lung spaces. Accepted: 5 March 1997  相似文献   

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Expiratory flow-volume curves with periodic interruption of flow showed flow transients exceeding maximal flow (Vmax) measured on the maximum expiratory flow-volume (MEFV) curve in a mechanical lung model and in five tracheotomized, vagotomized, open-chest, anesthetized dogs. Direct measurement of flow from the collapsing model airway showed that the volume of the flow transients in excess of the MEFV envelope was greater than that from the collapsing airway. Determination of wave-speed flows from local airway transmural pressure-area curves (J. Appl. Physiol. 52: 357-369, 1982) and photography of the airway led to the following conclusions. Flow transients exceeding Vmax are wave-speed flows determined by an initial and unstable configuration of the flow-limiting segment (FLS) with maximum compression in the midportion. The drop in flow from the peak to the following plateau is due to development of a more stable airway configuration with maximum compression at the mouthward end with a smaller area and a smaller maximal flow. When FLS jumps to a more peripheral position, the more distal airways may pass through similar configurational changes that are responsible for the sudden decrease of flow (the "knee") seen on most MEFV curves from dogs.  相似文献   

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The usual method of measuring density dependence of maximum expiratory flows is superimposition at total lung capacity or residual volume of maximum expiratory flow volume (MEFV) curves obtained breathing air and a mixture of 80% He plus 20% O2 (HeO2). A major problem with this technique is the large variability in results, which has been thought to be due to errors in matching lung volumes on both gases. Accordingly, we obtained MEFV curves breathing air and HeO2 using a bag-in-the-box system so that the curves breathing the two gas mixtures could be directly superimposed without removing the mouthpiece (isovolume). Ten healthy, nonsmoking subjects performed MEFV curves on each gas mixture for six consecutive experiments. We compared the increase in flow at 50% of vital capacity (delta Vmax50) and volume of isoflow (Viso) by superimposing and matching the MEFV curves at total lung capacity, at residual volume, and using the isovolume method. The variability of each method was assessed by the mean intersubject and intrasubject coefficients of variation. In all subjects, the mean delta Vmax50 and Viso as well as their corresponding coefficients of variation were not significantly different among the three methods. We conclude that, in healthy nonsmoking young adults, the method chosen for superimposing and matching MEFV curves has no effect on the variability of delta Vmax50 and Viso.  相似文献   

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To evaluate methods used to document changes in airway function during and after exercise, we studied nine subjects with exercise-induced asthma and five subjects without asthma. Airway function was assessed from measurements of pulmonary resistance (RL) and forced expiratory vital capacity maneuvers. In the asthmatic subjects, forced expiratory volume in 1 s (FEV1) fell 24 +/- 14% and RL increased 176 +/- 153% after exercise, whereas normal subjects experienced no change in airway function (RL -3 +/- 8% and FEV1 -4 +/- 5%). During exercise, there was a tendency for FEV1 to increase in the asthmatic subjects but not in the normal subjects. RL, however, showed a slight increase during exercise in both groups. Changes in lung volumes encountered during exercise were small and had no consistent effect on RL. The small increases in RL during exercise could be explained by the nonlinearity of the pressure-flow relationship and the increased tidal breathing flows associated with exercise. In the asthmatic subjects, a deep inspiration (DI) caused a small, significant, transient decrease in RL 15 min after exercise. There was no change in RL in response to DI during exercise in either asthmatic or nonasthmatic subjects. When percent changes in RL and FEV1 during and after exercise were compared, there was close agreement between the two measurements of change in airway function. In the groups of normal and mildly asthmatic subjects, we conclude that changes in lung volume and DIs had no influence on RL during exercise. Increases in tidal breathing flows had only minor influence on measurements of RL during exercise. Furthermore, changes in RL and in FEV1 produce equivalent indexes of the variations in airway function during and after exercise.  相似文献   

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Wave-speed theory predicts that maximal expiratory flow (MEF) at high lung volumes depends strongly on size of central airways. We tested this prediction by correlating MEF and tracheal cross-section area (T-XSA) in 15 (11 males, 4 females) healthy never-smoking volunteers. T-XSA was determined by planimetric analysis of contiguous 1-cm computerized tomographic scans of the intrathoracic trachea. We found a significant correlation between T-XSA at total lung capacity (TLC) and flow at 75% of vital capacity (V75) (r = 0.88, P less than 0.001). This contrasted to the correlation found between lung volume at TLC and V75 (r = 0.60). Density dependence of airflow (percent increase in V75 in air) was 35 +/- 17% and showed a significant inverse relationship to T-XSA (r = 0.70). These results confirm predictions of wave-speed theory and demonstrate the importance of cross-sectional area of central airways in determining MEF at high lung volumes. The large variability of MEF in normal individuals partly represents variations in tracheal size. Poor correlation between lung size and airway size suggests only a loose coupling between airways and lung parenchyma consistent with dysanaptic growth. Our findings indicate that changes in density dependence of airflow are not solely determined by the status of small airways and that differences in tracheal size contribute to its variability.  相似文献   

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During recent yearsit has been suggested that forced expiratory measurements, derived froma lung volume set by a standardized inflation pressure, are morereproducible than those attained during tidal breathing when the rapidthoracoabdominal compression technique is used in infants. The aim ofthis study was to evaluate the feasibility of obtaining measurementsfrom raised lung volumes in unsedated preterm infants. Measurementswere made in 18 infants (gestational age 26-35 wk, postnatal age1-10 wk, test weight 1.4-3.5 kg). Several inflations[1.5-2.5 kPa (15-25cmH2O)] were used to brieflyinhibit respiratory effort before the rapid thoracoabdominal compression was performed. Conventional analysis of flows and volumesat fixed times and percentages of the forced expiration resulted in arelatively high variability in this population. However, by using theelastic equilibrium point (i.e., the passively determined lung volume,derived from passive expirations before the forced expiration) as avolume landmark, it was feasible to achieve reproducible results inunsedated preterm infants, despite their strong respiratory reflexesand rapid respiratory rates. Because this approach is independent ofchanges in expiratory time, expired volume, or applied pressures, itmay facilitate investigation of the effects of growth, development, anddisease on airway function in infants, particularly during the firstweeks of life, when conventional analysis of forced expirations may be inappropriate.

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We determined the role of expiratory flow limitation (EFL) on the ventilatory response to heavy exercise in six trained male cyclists [maximal O2 uptake = 65 +/- 8 (range 55-74) ml. kg-1. min-1] with normal lung function. Each subject completed four progressive cycle ergometer tests to exhaustion in random order: two trials while breathing N2O2 (26% O2-balance N2), one with and one without added dead space, and two trials while breathing HeO2 (26% O2-balance He), one with and one without added dead space. EFL was defined by the proximity of the tidal to the maximal flow-volume loop. With N2O2 during heavy and maximal exercise, 1) EFL was present in all six subjects during heavy [19 +/- 2% of tidal volume (VT) intersected the maximal flow-volume loop] and maximal exercise (43 +/- 8% of VT), 2) the slopes of the ventilation (DeltaVE) and peak esophageal pressure responses to added dead space (e.g., DeltaVE/DeltaPETCO2, where PETCO2 is end-tidal PCO2) were reduced relative to submaximal exercise, 3) end-expiratory lung volume (EELV) increased and end-inspiratory lung volume reached a plateau at 88-91% of total lung capacity, and 4) VT reached a plateau and then fell as work rate increased. With HeO2 (compared with N2O2) breathing during heavy and maximal exercise, 1) HeO2 increased maximal flow rates (from 20 to 38%) throughout the range of vital capacity, which reduced EFL in all subjects during tidal breathing, 2) the gains of the ventilatory and inspiratory esophageal pressure responses to added dead space increased over those during room air breathing and were similar at all exercise intensities, 3) EELV was lower and end-inspiratory lung volume remained near 90% of total lung capacity, and 4) VT was increased relative to room air breathing. We conclude that EFL or even impending EFL during heavy and maximal exercise and with added dead space in fit subjects causes EELV to increase, reduces the VT, and constrains the increase in respiratory motor output and ventilation.  相似文献   

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We measured regional lung volumes from apex to base in humans during changes in thoracoabdominal shape which we monitored with magnetometers. In erect subjects, voluntary changes of shape at FRC did not change regional volume distribution. In supine subjects, the effect of negative pressure applied to the abdomen and a similar thoracoabdominal configuration achieved by voluntary means were studied. The distribution of regional volumes in both situations was the same as that measured during relaxation at the same overall lung volumes. We concluded that neither voluntary changes in shape nor negative abdominal pressure influenced the human pleural pressure gradient. This result, which differed from findings in animals, was probably because the human chest was relatively stiff and behaved with one degree of freedom; all parts of the human rib cage changed dimensions proportionally while negative abdominal pressure distorted the rib cage of animals.  相似文献   

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