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Biomedical subjects

C Veriter

Publications and source records attributed to C Veriter.

At least 37 records · Page 2Linked to original sources

Bronchodilator effect of inhaled nitric oxide in healthy men.

Studies in animals have shown that inhalation of nitric oxide (NO) either reduced pulmonary resistance after an induced bronchospasm or protected animals from bronchoconstriction. To evaluate whether NO inhalation (80 parts per million) influences basal bronchial tone or reverses methacholine-induced bronchospasm, we determined specific airway conductance (SGaw) as a measure of airway caliber in seven healthy men. After methacholine-induced bronchoconstriction NO increased SGaw by 23% (p < 0.05). One week later, NO inhalation did not change baseline SGaw values. However, albuterol inhaled after NO, or on a separate day, significantly increased SGaw (p < 0.05). The bronchodilator effect of NO in men with methacholine-induced bronchospasm is much less than that reported in animals or that regularly observed in asthmatic patients after the inhalation of beta-sympathomimetic drugs.

Administration, Inhalation↗

Contraction and relaxation of upper airway muscles during expiratory application of negative pressure at the mouth.

Upper airway muscles (UAM) are activated during inspiration, but little is known about their activity during expiration. We studied six healthy volunteers in supine position. Negative pressure (-10 to -30 cm H2O) was applied cyclically at the mouth during expiration. Subjects actively breathed during inspiration and either contracted or relaxed their UAM during expiration. Supraglottic pressure (Psg) was measured with a catheter with the tip at the supraglottic level. During relaxation, but not during contraction, there was expiratory flow limitation (FL) accompanied by high frequency pressure and flow oscillations (70 +/- 5.7 Hz at -30 cm H2O). The average linear supraglottic resistance was higher during relaxation than during contraction at both -10 and -20 cm H2O (p < 0.05), but not at -30 cm H2O. Amplitude of expiratory genioglossus electromyogram was 3.6 +/- 2.5 mm during quiet breathing, 7.0 +/- 3.8 mm during contraction (p < 0.05) and 4.1 +/- 1.8 mm during relaxation. Average mouth pressure, which immediately preceded pressure (and flow) oscillations was -2.1 +/- 0.9 cm H2O. In one subject cineradiography of the neck during expiratory application of -30 cm H2O showed anterior flexion and high frequency oscillations of the soft palate during relaxation. During contraction, the soft palate was close to the posterior pharyngeal wall without oscillations. We conclude that cyclically applied negative pressure at the mouth during expiration produced expiratory flow limitation during relaxation but not during contraction, and that expiratory contraction of UAM stabilizes upper airways during negative pressure application at the mouth.

Adult↗

Upper airway obstruction induced by negative-pressure ventilation in awake healthy subjects.

Negative-pressure ventilation (NPV) induces sleep-related upper airway obstruction. However, the precise mechanism and site of upper airway obstruction during NPV have not been worked out. We studied seven awake healthy volunteers (23-30 yr old) in an Emerson tank respirator. Subjects had the head outside the iron lung and breathed through a pneumotachograph, which yielded the airflow (V) signal. Supraglottic pressure (Psg) was measured with a catheter with the tip at the retroepiglottic level. Diaphragmatic electromyograms (EMGdi) were obtained from an esophageal bipolar electrode. Tidal volume was measured with an inductance plethysmograph. Measurements were done at -10, -20, and -30 cmH2O. At each pressure run subjects were asked to repeatedly relax or to actively breathe in phase with the respirator. Subjects had been previously trained to relax during NPV. During the relax runs there was no EMGdi activity. Stridor or wheezing occurred in all seven subjects during the relax runs but not during the active runs. Two patterns were associated with NPV during relax runs. One pattern was decreases in both V and Psg followed by zero values of these indexes, which corresponded to an inspiratory narrowing and closure of the glottis. These changes were visualized by fiber-optic bronchoscopy in one subject. The second pattern was a decrease in V and increase in Psg, which corresponded to an inspiratory supraglottic obstruction. In five subjects a supraglottic pattern was observed, whereas in two subjects glottic closure was seen. We conclude that muscular relaxation during NPV produces a decrease in the caliber of the upper airways at the glottic or supraglottic level. An uncoupling of upper airway muscle activity and the diaphragm might be the mechanism responsible for these changes.

Adult↗

Upper airway anesthesia induces airflow limitation in awake humans.

Upper airway receptors are thought to contribute to upper airway stability by reducing collapsing forces. Their activity can be abolished by topical anesthesia. We have measured in 16 healthy volunteers (mean +/- SD age, 23.7 +/- 1.6 yr) specific airway conductance (SGaw), maximal inspiratory (MIFR) and expiratory (MEFR) flow rates before and 15, 35, and 45 min after extensive upper airway anesthesia (UAA) with 10% lidocaine. Average values of MIFR decreased (p less than 0.01) 15 min after UAA, but they returned to or near to control values at 45 min: MIF25 (4.8 versus 6.0 L/s); MIF50 (5.1 versus 6.2 L/s); MIF75 (4.4 versus 5.3 L/s). Transient decreases in flow (V) rates, reaching zero flow in some subjects, were observed in 13 subjects during forced inspiratory vital capacity (FIVC) maneuvers and in seven subjects during forced expiratory vital capacity (FEVC) maneuvers. MEFR at 25, 50, and 75% FVC, SGaw, and FVC did not change after anesthesia. Simultaneous measurements of supraglottic pressure, V, and lung volume in 12 of the 16 subjects showed that the site of flow limitation was localized at the level of the glottis in all except one subject in whom there was both a glottic and a supraglottic obstruction. We conclude that extensive upper airway anesthesia induced a profound but transitory upper airway obstruction during FIVC and FEVC maneuvers. These findings are compatible with the concept of reflex regulation of upper airway caliber.

Adult↗

[The effect of inhaled salbutamol on pulmonary gas exchange in patients with chronic obstructive bronchopneumopathy].

The aim of this study is to establish whether or not the inhalation of a puff of salbutamol (Ventoline, 100 micrograms) could induce hypoxemia. Twenty-five chronic obstructive pulmonary disease (COPD) patients were investigated. In a first group of 20 patients arterial blood gases and related indices were measured before and 5, 10, 30, 60 and 90 minutes after inhalation of salbutamol. The oxyhemoglobin dissociation curve was traced before and 90 minutes after the drug intake. Except in two subjects in whom salbutamol dramatically improves arterial blood gases, the drug had no effect on the investigated parameters. It is concluded that salbutamol does not affect the blood gases in COPD patients. In this respect the behaviour of COPD patients differs from that of asthmatics in whom salbutamol generally induced hypoxemia.

Administration, Inhalation↗

Pattern of snoring in obstructive sleep apnea patients and in heavy snorers.

We measured respiratory mechanical characteristics during sleep in five heavy, nonapneic snorers (HS) and in five obstructive sleep apnea (OSA) patients. In two HS and in two OSA patients we obtained lateral pharyngeal cineradiographic images during sleep while snoring. Flow limitation preceded all snores in both HS and OSA. Pattern of snoring, hysteresis and temporal relationship between supraglottic pressure (Psg) and flow rate were different in HS and OSA. Maximal flow during snoring was less (p less than 0.05) in OSA (0.18 +/- 0.07 liter/second) than in HS (0.36 +/- 0.06 liter/second). Linear supraglottic resistance during inspiratory snoring was higher, though not significantly, in OSA patients (7.11 +/- 3.01 cm H2O/liter/second) than in HS (4.80 +/- 2.83 cm H2O/liter/second). We conclude that: 1) Snoring is characterized by high frequency oscillations of the soft palate, pharyngeal walls, epiglottis and tongue. 2) Flow limitation appears to be a sine qua non for snoring during sleep. 3) The pattern of snoring is different in OSA and HS. 4) Pharyngeal size during snoring is probably larger in HS than in OSA patients.

Adult↗

Pattern of simulated snoring is different through mouth and nose.

Cineradiography of the pharynx during simulated snoring was done in 6 healthy volunteers, and supraglottic pressure and flow rate were recorded in 12 others. We observed, immediately before snoring, a decrease in the sagittal diameter of the oropharynx followed, during snoring, by high-frequency oscillations of soft palate and pharyngeal walls. The pattern of soft palate oscillations was different while snoring through the nose or mouth. During inspiratory snoring through the nose, the soft palate remained in close contact with the back of the tongue and only the uvula presented high-frequency oscillations. Snoring through the mouth resulted in ample high-frequency oscillations of the whole soft palate. Frequency of airflow and supraglottic pressure oscillations was less (P less than 0.05) during mouth (28.2 +/- 7.5 Hz) than during nasal snoring (77.8 +/- 36.7 Hz). This difference may be related to the smaller oscillating mass (i.e., uvula) during nasal snoring. At variance with our previous data, which showed that snoring during sleep, in both heavy (nonapneic) snorers and obstructive sleep apnea patients, was systematically preceded by flow limitation, this was not true during simulated snoring.

Adult↗

Hypopharyngeal and neck cross-sectional changes monitored by inductive plethysmography.

We present a method to assess cross-sectional area (CSA) changes of the extrathoracic airways (EA) by using an inductive plethysmograph (IP) band placed around the upper part of the neck. Measurements of mouth pressure (Pm) (or flow rate, V) and neck CSA changes during respiratory efforts against a high (or infinite) resistance have shown a highly significant relationship between Pm changes (or V changes, respectively), reflecting CSA changes of the EA and CSA changes of the neck. Simultaneous measurements of CSA of the neck (by IP) and of EA (by computerized tomography) during sustained inspiratory and expiratory efforts against a closed airway showed a high correlation between changes in the former and latter structures. Changes in CSA of the neck were larger with positive than negative transmural pressures, in keeping with the known larger compliance of this airway during expiration. We found this method helpful to assess the behavior of the EA during obstructive apnea episodes, hypopneas, and snoring.

Adult↗

Effects of two inotropic drugs, dopamine and dobutamine, on pulmonary gas exchange in artificially ventilated patients.

The inotropic agents, dopamine (DP) and dobutamine (DB), both decrease PaO2, probably by a redistribution of the VA/Q ratio. The aim of this study was to assess the effect of both drugs on the VA/Q ratio, using the multiple inert gas elimination method. Ten artificially ventilated patients (eight males), aged 45-74 years were investigated. Blood gases, cardiac output and concentrations of inert gases were measured before and 30 min after infusion of DB or DP. DP and DB were administered alternatively at a rate of 5 micrograms.k-1 min-1. The decrease in PaO2 was significantly greater with DP (12 +/- 9 torr) than with DB (7 +/- 9 torr) (P less than 0.01). Both drugs similarly increased cardiac output: +2.61.min-1 +/- 1.4 for DP and 2.21.min-1 +/- 1.5 for DB. Both DP and DB significantly (P less than 0.01) increased the perfusion of alveoli with VA/Q = 0 (+4 +/- 7% for DP and +3 +/- 7% for DB) and 0 less than VA/Q less than 0.1 (+11 +/- 8.5% for DP and +5.5 +/- 10.5% for DB) (no significant difference between the drugs). When shunt and "shunt-like" effect are considered together, there was a significantly greater increase in the amount of blood going to alveoli with a low VA/Q ratio with DP compared to DB. Both drugs decreased the perfusion of alveoli with 0.1 less than VA/Q less than 10, but the decrease was significantly less for DB than for DP (-15 +/- 6.5% for DP and -8.5 +/- 7% for DB, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Reassessment of the interruption technique for measuring flow resistance in humans.

We have previously produced evidence that, in patients with obstructive lung disease, compliance of extrathoracic airways is responsible for lack of mouth-to-alveolar pressure equilibration during respiratory efforts against a closed airway. The flow interruption method for measuring respiratory resistance (Rint) is potentially faced with the same problems. We reassessed the merits of the interruption technique by rendering the extrathoracic airways more rigid and by using a rapid shutter. We measured airway resistance (Raw) with whole body plethysmography during panting (at 2 Hz) and Rint during quiet breathing. Rint and Raw were expressed as specific airway (sGaw) and interruptive conductance (sGint), respectively. In nine healthy subjects (cheeks supported), sGint (0.140 +/- 0.050 s-1.cmH2O-1) was lower (P less than 0.02) than sGaw (0.182 +/- 0.043 s-1.cmH2O-1). By contrast, in 12 patients with severe obstructive lung disease (forced expiratory volume in 1 s/vital capacity = 41.0 +/- 19.8%), sGint (0.058 +/- 0.012 s-1.cmH2O-1) was higher (P less than 0.05) than sGaw (0.047 +/- 0.007 s-1.cmH2O-1), when the cheeks were supported. When the mouth floor was also supported, average values of sGaw (0.048 +/- 0.008 s-1.cmH2O-1) and sGint (0.049 +/- 0.014 s-1.cmH2O-1) became similar. In conclusion, we confirm previous findings in healthy subjects of higher values of Rint, with respect to Raw, probably because of differences in glottis opening between quiet breathing and panting. In airflow obstruction, supporting both the cheeks and the mouth floor decreased sGint, which became similar to sGaw.

Adult↗

Pulmonary gas exchange during graded exercise in normal, sedentary, non-smoking subjects.

There is some discordance in the literature on the evolution of the alveolo-arterial oxygen tension difference (A-a)DO2 from rest (R) to graded exercise (E) in healthy subjects. For some authors and not for others (A-a)DO2 increased during exercise. In order to solve this problem we have examined 9 healthy, non-smoking sedentary students (5 males). In every subject PaO2 increased from rest to the highest level of exercise. (A-a)DO2 significantly increased from R and E1 to E2 and from E3 to E4. (A-a)DO2 at rest was 7.5 +/- 4.1 torr; at E1: 7.0 +/- 4.3 torr; at E2: 11.5 +/- 4.2 torr; at E3: 12.5 +/- 3.9 torr; and at E4: 16.5 +/- 4.3 torr. The oxyhemoglobin dissociation curve (ODC) was significantly shifted to the right from 53 to 92% saturation. This shift favours the liberation of O2 from hemoglobin to the tissues but cannot explain the evolution of (A-a)DO2. We believe that the increase in (A-a)DO2 is due to an increased maldistribution of the ventilation-perfusion ratio.

Adult↗

Head position modifies upper airway resistance in men.

We measured in healthy volunteers airway resistance (R(aw)), resistance of the respiratory system (Rrs), and supralaryngeal resistance (Rsl) in the following head positions: neutral, extended, and partially and fully flexed. Sagittal magnetic resonance images of the upper airways were recorded in neutral and flexed head positions. We observed significant increases in Raw (P less than 0.01), Rrs (P less than 0.001), and Rsl (P less than 0.001) in the flexed position, with respect to the neutral one, and corresponding decreases of specific airway and specific respiratory conductances. Resistances decreased (although not significantly) when the subjects' heads were extended. A decrease in both diameter and surface area of the hypopharyngeal airways (as shown by magnetic resonance images) with total head flexion was accompanied by significant increases in all measured resistances. Changes in the caliber of hypopharynx appear to be responsible for the increase in resistance during head flexion.

Adult↗

Ventilatory and diaphragmatic EMG responses to negative-pressure ventilation in airflow obstruction.

To assess the responses of patients with chronic obstructive lung disease (COLD) to negative-pressure ventilation (NPV), we studied eight naive patients with moderate to severe COLD before (control) and during NPV with "low" (-10-cmH2O) and "high" (-30-cmH2O) pressure swings in a Drinker tank respirator. Tidal volume (VT) and minute ventilation (VE) were recorded from a Respitrace and diaphragmatic electromyogram (DEMG) from a bipolar esophageal electrode. During short, 5-min runs of "low" and "high" NPV, VT did not change and VE increased in a borderline significant way at -30-cmH2O NPV. Peak integrated DEMG amplitude did not change with respect to control during short runs of NPV. However, when NPV was maintained for 20-60 min, a significant (though small, 20%) decrease in peak DEMG amplitude was observed with respect to control. By contrast, in a ninth patient habituated to NPV, the decrease in peak DEMG amplitude during a 5-min run of NPV was 60%. Significant increases in arterial PO2 (at -10- and -30-cmH2O NPV) and decreases in arterial PCO2 (at -30-cmH2O NPV) were found during NPV for the whole group of patients. One-to-one phase locking between the respirator and patients was the most common pattern of entrainment observed. However, 1:1 phase locking did not preclude the presence of dissociation between the two pacemakers. We conclude that short runs of NPV in naive patients do not result in changes in DEMG, as opposed to immediate and nearly complete cessation of inspiratory activity in trained patients.

Diaphragm↗

Impairment of ventilatory function and pulmonary gas exchange in non-smoking coalminers.

Indices of ventilatory function and pulmonary gas exchange in 32 non-smoking coalminers (mean age 38.1) were compared with those of 34 non-smoking steelworkers of similar age. The coalminers had significantly lower forced expiratory volume in 1 s (FEV1) and maximum expiratory flow rates and significantly higher residual volume, but similar vital capacity and indices derived from the single-breath test. Pulmonary diffusing capacity for CO and indices of CO2 exchange were similar in both groups. Arterial partial pressure of O2 (PaO2) was significantly lower and alveolar-arterial O2 difference was significantly higher in coalminers than in controls, both at rest and during exercise. There was no relation between lung function and radiological signs of simple pneumoconiosis (10 coalminers had pneumoconiosis). The differences in FEV1 (0.42 l) and in PaO2 (10 mm Hg) between the two groups are the same or larger than those usually found between smokers and non-smokers. Exposure to coaldust may result in biologically significant alterations of lung function even in the absence of pneumoconiosis.

Adult↗

Hysteresis of the alveolar capillary membrane in normal subjects.

Weibel and associates (Respir. Physiol. 18: 285-308, 1973), using morphometric techniques, demonstrated in the rat that changes in lung volume related to inflation and deflation caused a hysteretic variation in alveolar capillary membrane which is locally pleated at low pulmonary volume, unfolds during inflation but does not immediately refold during deflation, possibly enhancing the CO diffusion throughout the membrane. The present study was conducted to verify the existence of this hysteresis in human lungs in vivo. Single-breath diffusing capacity for CO (DLCO) was measured in five healthy seated subjects before and 0, 0.5, 1, 3, and 7 min after an inflation-deflation maneuver (IDM) in 6 separate days. The value of mean DLCO was 36.4 +/- 3 (SD) before and 42.1 +/- 2.9, 41.6 +/- 3.3, 40.3 +/- 3.3, 39.2 +/- 3.2, and 38.1 +/- 2.7 ml X min-1 X Torr-1 after the IDM. Two mechanisms can explain our findings: an active filling of the capillary bed, or an unfolding of the alveolar capillary membrane. The first mechanism should be accompanied by changes in pulmonary circulation. Therefore, right-heart catheterization was performed in two normal subjects and in four patients examined for a chest pain syndrome. At the end of the IDM, the values for the pulmonary artery pressure and capillary wedge pressure had returned to control levels. This suggests that the capillary bed is not directly involved in the DLCO increase observed from 0.5 to 7 min after the IDM. The unfolding of the alveolar capillary membrane appears to better explain our findings.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗

Lung function measurements over 21 days shiftwork in steelworkers from a strandcasting department.

On the assumption that short term changes in lung function may reflect the potential for a long term decline the evolution of lung function indices in 25 steelworkers from a strandcasting department and in 11 comparable steelworkers not exposed to dust was investigated over an almost uninterrupted 21 day working period and over three different workshifts. The mean total dust level in the strandcasting department, assessed by personal sampling, was 11.8 mg/m3. All subjects were examined at the beginning, in the middle, and at the end of their first (day 1) morning shift (0600 to 1400), their last (day 14) afternoon shift (1400 to 2200), and their last (day 21) night shift (2200 to 0600). Indices measured were vital capacity (VC), forced expiratory volume in one second (FEV1) and in three seconds (FEV3), forced expiratory flow over the middle half of the forced vital capacity (FEF25-75), peak expiratory flow rate (PEFR), the slope of the N2 plateau (delta N2) and the closing volume (CV) of the single breath oxygen test. Differences in indices between initial values (0600 on day 1) and final values (0500 on day 21) were not significant in the control group (except delta N2 which became lower); in the casting group there were significant (p less than 0.05) decreases in FEF25-75 and FEV3, but these decreases were not significantly greater than in the control group. Lung function changes were not significant in either group over the morning shift. During the afternoon there were significant decreases in spirometric indices in the casting group, with no significant decreases in the control group, but the interactions between exposure and time were generally not significant. During the night shift, however, the decreases in FEV1 and FEF25-75 observed in the strandcasting group were significantly more pronounced than in the control group. The single breath test, which many subjects failed to perform correctly on each occasion, showed no significant changes in closing volumes, and an "improvement" of delta N2 over the morning and the night shift in the control but not the exposed subjects needs to be interpreted with caution. The more pronounced decrease in spirometric indices, suggestive of slight airways obstruction, found over the night shift in the strandcasting workers is attributed to their working environment.

Belgium↗

Effects of gas density on pulmonary gas exchange of normal man at rest and during exercise.

Changes in the physical properties of inspired gas might be expected to influence the distribution of ventilation in the lungs as well as the diffusive and convective (cardiogenic) mixing of inspired gas with lung residual gas, thus possibly affecting pulmonary gas exchange for O2 and CO2. The purpose of our work was to assess to what extent this occurs in practise in human subjects, who could compensate for the changes directly brought about by altering the physical characteristics of the inhaled gas by changing their breathing pattern. Six healthy, non-smoking men breathed, at rest and during moderate exercise, gas mixtures containing 21% oxygen completed either by 79% nitrogen (air), helium (O2-He) or sulphur hexafluoride (O2-SF6). We observed that the inhalation of these three different gas mixtures whilst at rest did not affect arterial partial pressures of O2 or CO2, the physiological dead space to tidal volume ratio, or the alveolo-aADCO2). During exercise, AaDO2 was slightly (2-3 mm Hg) but significantly higher with both O2-He and O2-SF6 than with air. Although minute ventilation did not change, breathing frequency was slightly but significantly affected by the type of gas mixture breathed, being lower with O2-SF6 and higher with O2-He. We conclude that, within the range studied, the physical properties of the inhaled gas do not affect pulmonary gas exchange in healthy man, either because the changes affected are minimal or because they compensate for each other.

Adult↗