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Biomedical subjects

N Zamel

Publications and source records attributed to N Zamel.

At least 109 records · Page 6Linked to original sources
PubMed1986

Maximum flow ratios at mid-vital capacity in young healthy adults.

Upper airway obstruction is usually diagnosed by visual examination of maximum expiratory and inspiratory flow-volume curves and by calculating a ratio of expiratory to inspiratory flow at 50 percent of vital capacity (mid-vital capacity flow ratio); however, reference values of this ratio have not been well established, and considerable variability exists. The purpose of this study was to examine the range of mid-vital capacity flow ratios in a group of healthy subjects and to determine if some of the variability is accounted for by different maximum inspiratory pressures. We measured maximum expiratory and inspiratory flows at 50 percent of vital capacity from the flow-volume curves, and maximum inspiratory pressures in a group of 60 healthy nonsmokers (30 men and 30 women) whose ages ranged from 21 to 40 years. We found that mid-vital capacity flow ratio (mean +/- SD) was 0.72 +/- 0.19 in men and 0.77 +/- 0.18 in women. The coefficient of variation of the mid-vital capacity flow ratio was 28 percent for men and 23 percent for women. The 95 percent confidence limits for the mid-vital capacity flow ratio were 0.65 to 0.79 for men and 0.70 to 0.84 for women. Maximum inspiratory pressures (mean +/- SD) were 129 +/- 30 cm H2O in men and 91 +/- 16 cm H2O in women, not significantly different from previous studies. Normalizing maximum inspiratory flow for maximum inspiratory pressure did not reduce the coefficient of variation, which became 29 percent in men and 30 percent in women. We conclude that the range of mid-vital capacity flow ratios is wide, and it cannot be reduced by standardizing it for maximum inspiratory pressures.

Adult↗
PubMed1985

Thoracoabdominal motion during hypercapnia, hypoxia, and exercise.

We measured, in 11 healthy volunteers, the contributions of rib cage and abdomen--diaphragm compartments to increased ventilation caused by hypercapnia, hypoxia, and exercise to determine whether different stimuli produce similar or different patterns of ventilation with respect to the motion of rib cage and abdominal compartments. Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia were induced by rebreathing methods and graded exercise performed on a treadmill, and compartmental tidal volume (VT) was measured by respiratory inductive plethysmography. For each stimulus, the wide range of VT responses among individuals was determined primarily by the range of rib cage contributions to VT, the abdominal compartment VT response slopes accounting for less of this range. There were no significant differences between hypercapnia and hypoxia in either rib cage or abdominal contributions to ventilation (for both, p less than 0.3). However, exercise rib cage and abdominal contributions to ventilation were significantly different from those during chemically driven breathing: for the rib cage compartment, p less than 0.0001 and for the abdominal compartment, p less than 0.05. Whereas, in 8 of 10 subjects the rib cage contribution to VT during exercise was similar to or exceeded that during rebreathing, in 7 of 10 subjects the abdomen-diaphragm contribution fell below that measured during both hypercapnia and hypoxia. There was a significant correlation between hypercapnia and hypoxia in the VT contribution of each compartment at equivalent levels of ventilation (rib cage, p less than 0.0001; abdomen, p less than 0.0005), but there was no significant correlation in the VT contribution of either compartment between exercise and hypercapnia or exercise and hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1985

Laryngeal constriction in normal humans during experimentally induced bronchoconstriction.

Changes in the size of the glottis with bronchoconstriction were assessed in six normal subjects following inhalation of histamine or methacholine. Measurements were made during both tidal breathing and panting at 2-3 Hz. The midexpiratory size of the glottis was decreased by a mean of 8% during bronchoconstriction compared with control during tidal breathing. Changes in midinspiratory size were inconsistent. During panting, the glottic size was unchanged from inspiration to expiration but decreased in 7 of 15 studies during bronchoconstriction. The decreases in expiratory size of the glottis during quiet breathing would lead to an elevated laryngeal resistance coupled with an increased lower airway resistance. Although this seems to be a paradoxical laryngeal response, it may contribute to maintaining hyperinflation during bronchoconstriction, thereby effectively enlarging the lower airways.

Adult↗
PubMed1985

Failure of cholinergic blockade to prevent bronchodilatation following deep inspiration.

The role of the cholinergic system in the phenomenon of bronchodilatation following a deep inspiration (BDFI) in humans has not been well established, although animal studies have suggested the cholinergic system to be of prime importance. We therefore induced cholinergic blockade with inhaled ipratropium bromide (Sch-1000) in five asymptomatic subjects and then assessed whether BDFI had been abolished. Since BDFI is only evident where there is normal or increased bronchomotor tone, prostaglandin F2 alpha (PGF2 alpha), a noncholinergic bronchoconstrictor, was used to re-establish bronchomotor tone in the presence of cholinergic blockade. At each stage the presence or absence of BDFI was assessed by comparing flows from a partial forced expiratory maneuver started at approximately 60% of vital capacity (Vmaxp) with flows from a forced expiratory maneuver started at lung capacity (Vmaxc). Flows were measured at the last 40% of vital capacity. The percent ratio of Vmaxp/Vmaxc was used as an indicator of BDFI. In the presence of cholinergic blockade and with reestablishment of bronchomotor tone with PGF2 alpha, BDFI could still be demonstrated (Vmaxp/Vmaxc percent ratio: control 110.3 +/- 10.6, after Sch-1000 129.4 +/- 10.3, after Sch-1000 and PGF2 alpha 59.4 +/- 6.9; P = 0.001). We conclude that there is not an essential role for the cholinergic system in the phenomenon of BDFI in healthy individuals.

Adult↗
PubMed1985

Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea.

Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). All patients underwent pulmonary function testing, arterial blood gas analysis, and overnight polysomnography. Mean nocturnal SaO2 ranged from 96 to 66% and apnea-hypopnea index from 11 to 128 per hour of sleep. Several anthropometric, respiratory physiological, and polysomnographic variables that could be expected to influence nocturnal SaO2 were entered into a stepwise multiple linear regression analysis, with mean nocturnal SaO2 as the dependent variable. Three variables [awake supine arterial PO2 (PaO2), expiratory reserve volume, and percentage of sleep time spent in apnea] were found to correlate strongly with mean nocturnal SaO2 (multiple R, 0.854; P less than 0.0001) and accounted for 73% of its variability among patients. Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.

Adult↗
PubMed1985

Lung volume dependence of esophageal pressure in the neck.

There is conflicting evidence in the literature regarding tissue pressure in the neck. We studied esophageal pressure along cervical and intrathoracic esophageal segments in six healthy men to determine extramural pressure for the cervical and intrathoracic airways. A balloon catheter system with a 1.5-cm-long balloon was used to measure intraesophageal pressures. It was positioned at 2-cm intervals, starting 10 cm above the cardiac sphincter and ending at the cricopharyngeal sphincter. We found that esophageal pressures became more negative as the balloon catheter moved from intrathoracic to cervical segments, until the level of the cricopharyngeal sphincter was reached. At total lung capacity, esophageal pressures were -10.5 +/- 2.9 (SE) cmH2O in the lower esophagus, -18.9 +/- 3.0 just within the thorax, and -21.3 +/- 2.73 within 2 cm of the cricopharyngeal sphincter. The variation in mouth minus esophageal pressure with lung volume was similar in cervical and thoracic segments. We conclude that the subatmospheric tissue pressure applied to the posterior membrane of the cervical trachea results in part from transmission of apical pleural pressure into the neck. Transmural pressure for cervical and thoracic tracheal segments is therefore similar.

Adult↗
PubMed1985

Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome.

Although right heart failure is a recognized complication of obstructive sleep apnea, the incidence and pathogenesis of this complication have not been established. We therefore studied 50 consecutive patients with obstructive sleep apnea to determine the incidence of right heart failure and the factors involved in its development. Six patients (12%) were found to have right heart failure. There were no differences in the number of apneas between those with right heart failure (mean +/- SE, 30 +/- 10 per h sleep) and those without right heart failure (33 +/- 4 per h sleep). In contrast, mean nocturnal oxygen saturation was lower in patients with right heart failure (76 +/- 3%) than in those without right heart failure (90 +/- 1%; p less than 0.001). Furthermore, patients with right heart failure also had a substantially lower awake arterial PO2 (52 +/- 4 mmHg versus 75 +/- 2 mmHg; p less than 0.001) and a higher PCO2 (51 +/- 2 mmHg versus 36 +/- 1 mmHg; p less than 0.001) than those without right heart failure. Severe nocturnal hypoxemia in the absence of diurnal hypoxemia was not associated with right heart failure. Daytime hypoxemia in the patients with right heart failure was associated with a higher residual volume (p less than 0.001) and lower forced expiratory volume in one second (p less than 0.001) than in the patients without right heart failure. The findings suggest that sustained hypoxemia and/or hypercapnia over a 24-h period is a necessary prerequisite for the development of right heart failure in patients with obstructive sleep apnea, and that diffuse airway obstruction plays a major role in causing such hypoxemia.

Circadian Rhythm↗
PubMed1985

Pharyngeal compliance in snoring subjects with and without obstructive sleep apnea.

Recent studies have demonstrated a reduction in pharyngeal cross-sectional area and in upper airway muscle tone in patients with obstructive sleep apnea. These findings suggest that the pharynx in such patients may be more compliant than normal even in the awake state. We have tested this hypothesis by examining the pressure-area relationship of the pharynx in 13 patients and in 7 control subjects. Measurements were performed during wakefulness, with the subject seated, and at a constant lung volume near functional residual capacity. Pharyngeal area was measured by an acoustic reflection technique. Pharyngeal pressure was varied by having the subject perform gradual inspiratory and expiratory isovolume maneuvers against a distally occluded airway while mouth pressure was recorded. Specific compliance of the pharynx was calculated as the fractional change in pharyngeal area between a pressure of 0 and -10 cm H2O and and between 0 and 10 cm H2O. Specific pharyngeal compliance was 0.036 +/- 0.004 cm H2O-1 (mean +/- SE) in the control group and 0.094 +/- 0.012 cm H2O-1 in patients with OSA (p less than 0.01). These findings indicate that patients with obstructive sleep apnea have increased pharyngeal compliance. This abnormality predisposes to pharyngeal occlusion during sleep when negative transmural pressures are generated in the pharynx.

Acoustics↗
PubMed1985

Limited bronchoconstriction to methacholine using partial flow-volume curves in nonasthmatic subjects.

We investigated whether the plateau of the dose-response to nonsensitizing stimuli, such as methacholine, could be explained by the airway dilation that follows lung inflation in nonasthmatics. We used maximal expiratory partial flow-volume curves to measure the response of the airways to doubling doses of inhaled methacholine up to 256 mg/ml (a noncumulative dose of 340 mumol delivered to the mouth during tidal breathing) in 12 nonasthmatics on 2 days. Maximal expiratory complete flow-volume curves and FEV1 were also obtained along with the partial curves. Flows were measured at 40% of control vital capacity using the complete (V40c) and the partial (V40p) curves. A maximal response plateau of 2 or more doubling concentrations was demonstrated in all subjects based on V40p, and in 10 subjects based on FEV1. The level of the plateau was the highest for the V40p (mean +/- SD = 65 +/- 19% of baseline), intermediate for V40c (45 +/- 22%), and the lowest for FEV1 (16 +/- 11%). There was more than a 100-fold range in responsiveness expressed as the provocative concentration to cause a 40% fall of baseline in V40p (PC40); the lower the PC40, the higher the level of the plateau. All the results were reproducible between the 2 days. We also investigated whether the plateau may have been due to a tachyphylactic effect of cumulative doses of methacholine. The maximal response after increasing concentrations of methacholine up to 256 mg/ml was not different from the response obtained after a single dose of 256 mg/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Limited maximal airway narrowing in nonasthmatic subjects. Role of neural control and prostaglandin release.

In nonasthmatic subjects with normal airway responsiveness to methacholine, maximal airway narrowing is limited to a mild or moderate degree. We investigated whether the maximal response plateau or the position of the dose-response curve is due to functional inhibition by neurogenic mechanisms or to prostaglandin release. Four nonasthmatics inhaled doubling concentrations of methacholine up to 256 mg/ml (67 mg delivered during tidal breathing), followed by 4-fold-increasing doses of salbutamol up to 80 mg/ml (24 mg during tidal breathing) on 5 separate days. On each day 30 min before the test, the subjects inhaled (using a dosimeter) saline, propranolol (11 mg), or hexamethonium (910 mg) or, 2 h before the test, ingested indomethacin (75 mg) or placebo. The response to methacholine was measured from volume history standardized partial and complete maximal expiratory flow-volume curves, as FEV1 and the flows at 40% of the control FVC (V40p and V40c). Compared with saline, on average, baseline V40p was 18% lower after propranolol and 18% higher after hexamethonium. Indomethacin did not affect baseline values. There was no systematic difference between the 5 days in the dose of methacholine to cause a 10% fall in FEV1 or a 40% fall in V40p, or in the maximal response with FEV1, V40p, and V40c, or in V40p/V40c at 256 mg/ml methacholine. We conclude that limited maximal airway narrowing to methacholine in nonasthmatics is not due to a change in adrenergic, cholinergic, or ganglion-transmitted-nonadrenergic inhibitory activity nor to the release of prostaglandins.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Exercise-induced bronchodilation in asthma.

Of 34 symptomatic adult asthmatic patients (23 men) aged 51 +/- 13 years (mean +/- 1 SD) with moderately severe airways obstruction who underwent maximal exercise testing at room temperature (22 degrees C) and humidity (44 percent RH) using a bicycle ergometer, we identified seven male patients aged 56 +/- 9 years in whom forced expired volume in one second (FEV1) increased greater than or equal to 20 percent over the baseline pre-exercise value (exercise-induced bronchodilation). At maximal exercise, these patients achieved an O2 consumption of 1.4 +/- 0.4 L/min and a minute ventilation of 56 +/- 9 L/min. Baseline FEV1 was 1.3 +/- 0.5 L (SD) (43 +/- 12 percent predicted) and increased to 2.1 +/- 0.5 L at five minutes after exercise and persisted at least 20 minutes. Exercise was repeated in all seven patients on a separate day one to six months later, and results were similar in six. In these seven patients, three minutes of voluntary isocapnic hyperventilation achieving a minute ventilation comparable to that during maximal exercise led to an increase in FEV1 of 20 +/- 18 percent (range 0 to 54 percent). The Vmax50 was 22 +/- 30 percent before, and 10 +/- 21 percent after maximal exercise and 25 +/- 37 percent before, and 11 +/- 22 percent after isocapnic hyperventilation. Pre-treatment with acetylsalicylic acid (mean serum concentration 120 +/- 64 micrograms/ml) in the six patients with reproducible bronchodilation completely blocked exercise bronchodilation in one patient and blunted it in four others. Findings suggest that a subset of adult patients with symptomatic asthma may develop bronchodilation after six to eight minutes of exercise, that exercise-induced bronchodilation may in part be reproduced with isocapnic hyperventilation, and that it may be blocked completely or partially by acetylsalicylic acid, implying mediation by prostaglandins.

Aspirin↗
PubMed1984

Threshold of airway response to inhaled methacholine in healthy men and women.

Threshold of airway response to inhaled methacholine was determined using maximum expiratory partial flow-volume curves in 21 men and 36 women with similar age distribution, all of them healthy nonsmokers. Mean threshold was on average 1.3 doubling dose lower in women than men. There were no sex differences in the increase of maximum expiratory flows after a full inspiration when the airways were constricted by methacholine.

Adolescent↗
PubMed1984

Airway response to inhaled methacholine in healthy nonsmoking twins.

The variability of maximum expiratory flows is genetically determined, and the airway response to chronic cigarette smoking is also influenced by genetic factors. In nonsmoking nonatopic healthy individuals there is a wide variability of acute airway responses to bronchoactive drugs. The present study was designed to investigate whether this variability might also be genetically determined. We tested this hypothesis by measuring the threshold of airway response to inhaled methacholine using a partial flow-volume curve as the index of response in 10 monozygotic (MZ) and 10 dizygotic (DZ) healthy nonsmoking pairs of twins. Methacholine aerosol was given in doubling doses from number 1 (0.031 mg/ml) to number 11 (32 mg/ml). The mean threshold (+/-SD) for the MZ twins was dose 4.5 +/- 2.4 and for the DZ twins was 7.2 +/- 2.0 (P = 0.0004). No explanation could be found for the difference in mean threshold between MZ and DZ twins. The mean intrapair difference in threshold (+/-SD) for the MZ twins was 2.7 +/- 1.6 doubling doses and for the DZ twins was 2.4 +/- 1.8 (P = 0.7). Slope of dose response to methacholine and intrapair differences were not different between MZ and DZ twins. The present study supports the view that environmental factors are more important than genetic factors in determining the variability of acute airway responsiveness to bronchoactive drugs in healthy nonsmoking individuals.

Adolescent↗
PubMed1984

An efferent pathway mediating reflex tracheal dilation in awake dogs.

Lung inflation is known to produce reflex relaxation of tracheal smooth muscle (TSM) and dilation of the upper airway, but the specific efferent pathway involved has not been established. Therefore we examined TSM tone in four trained awake dogs by measuring pressure changes in the water-filled cuff of an endotracheal tube that was inserted into the lower cervical trachea through a permanent tracheostomy. Under control conditions, sustained lung inflation with 1 liter of air produced apnea (Hering-Breuer inflation reflex) and a decrease in cuff pressure (Pcuff) of 37.4 +/- 12.0 (mean +/- SD) cmH2O. beta-Adrenergic blockade with propranolol had no effect on either the apneic or TSM responses to lung inflation. Efferent parasympathetic blockade with atropine sulfate (1.2-2.4 mg) abolished TSM tone, which was then restored to control levels by a continuous intravenous infusion of serotonin (14-28 micrograms X kg-1 X min-1). Under these conditions, lung inflation still induced reflex apnea but no longer relaxed TSM tone (mean decrease in Pcuff, 2.7 +/- 1.4 cmH2O, P less than 0.001). The findings indicate that reflex tracheal dilation in response to lung inflation is mediated by an efferent cholinergic (parasympathetic) pathway.

Adrenergic beta-Antagonists↗
PubMed1984

Effects of cigarette smoking and short-term smoking cessation on airway responsiveness to inhaled methacholine.

Threshold of airway responsiveness to methacholine aerosol was determined in 53 apparently healthy persons. In 18 nonallergic nonsmokers matched according to sex and age to 18 nonallergic smokers, the mean methacholine threshold of airway response (T), as measured using partial flow-volume curves, had a tendency to be greater in nonsmokers, but the difference was not significant for the group as a whole; it was, however, significant for a subset of 9 matched pairs with a cigarette consumption greater than 10 pack-years (mean T nonsmokers, 2.8 mg/ml; smokers, 0.3; p = 0.036). In 17 smokers who stopped smoking for 99 days in average, T was not significantly different for the group as a whole, although the majority of the smokers reported improvement of respiratory symptoms after cessation of smoking. The results of this study indicate that cigarette smoking is associated with increased airways responsiveness to inhaled methacholine and that this effect is dose related.

Adult↗
PubMed1984

Combined effect of cigarette smoking and allergic rhinitis on airway responsiveness to inhaled methacholine.

A group of healthy nonatopic subjects was compared with a group of atopic subjects with allergic rhinitis who were otherwise healthy. They were matched for sex, age, and smoking habits; 15 pairs were nonsmokers and 11 pairs were smokers. Threshold of airway response to inhaled methacholine based on partial flow-volume curves was not significantly different between nonatopic nonsmokers and nonsmokers with allergic rhinitis. However, smokers with allergic rhinitis had a threshold on the average of 3 doubling doses lower than smokers without allergic rhinitis. We concluded that there is a combined effect of chronic cigarette smoking and allergic rhinitis affecting nonspecific airway responsiveness.

Adult↗