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Biomedical subjects

R E Hyatt

Publications and source records attributed to R E Hyatt.

At least 37 records · Page 2Linked to original sources
PubMed1987

Respiratory impedance in normal humans: effects of bronchodilatation and bronchoconstriction.

Total respiratory resistance and reactance from 3 to 30 Hz were determined by the method of forced random noise oscillation in 12 normal male subjects before and after bronchodilatation and bronchoconstriction induced by deep breaths of aerosols of isoproterenol and atropine and of methacholine and histamine. Isoproterenol and atropine induced small decreases in total respiratory resistance at most frequencies, and isoproterenol decreased resonant frequency slightly (P less than 0.01). After administration of both methacholine and histamine, resonance frequency increased (P less than 0.01) and total respiratory resistance became more frequency-dependent, increasing mainly in the lower frequency range. In six of the subjects, we attempted to produce central deposition of methacholine by rapid, shallow breathing and peripheral deposition of the drug by slow, deep breathing. Only two subjects had suggestive evidence of central bronchoconstriction. No difference was noted, however, in the impedance behavior with either type of breathing. In awake humans, impedance analysis does not seem to distinguish between central and peripheral airway constriction.

Adult↗
PubMed1987

Effect of effort on measurement of forced expiratory volume in one second.

The American Thoracic Society recommends that the largest FEV1 be reported from a set of forced expiratory vital capacity maneuvers performed with maximal expiratory effort. However, increased expiratory effort can decrease the FEV1. When we evaluated the peak expiratory flow rate (PEFR) in 5 normal subjects, measured from flow-volume curves, as a noninvasive index of expiratory effort, it was positively correlated with indices of effort obtained by using an esophageal balloon. We then measured the difference (dFEV1)between the largest FEV1 and FEV1 from the maneuver with the highest PEFR during 10 test sessions in 10 normal subjects. Thus, dFEV1 was always greater than or equal to 0. The mean dFEV1 was 110 ml for all sessions but decreased to 80 ml when maneuvers with poorly reproducible PEFR or forced expiratory vital capacity values were discarded. We also reviewed 9.471 spirometry sessions from outpatients and found dFEV1 to be greater than 50 ml in 26% of this population and greater than 151 ml in 7%. We concluded that during standard spirometry, FEV1 is inversely dependent on effort. Maximal effort decreases FEV1 because of the effect of thoracic gas compression on lung volume. We recommend that values from spirometry maneuvers that demonstrate submaximal effort, indicated by a decreased PEFR, be discarded. The flow-volume curve display of superimposed efforts facilitates the recognition of submaximal efforts.

Biophysical Phenomena↗
PubMed1986

Bronchiolitis in a rheumatoid arthritis patient receiving auranofin.

A patient with severe rheumatoid arthritis and sicca symptoms was treated with auranofin. During auranofin therapy, she developed irreversible airways obstruction due to bronchiolitis. Whereas this complication could have been due to her underlying disease, we discuss here the possibility of its being related to the auranofin therapy.

Adult↗
PubMed1986

Immunologic response to aerosols of affinity-purified antigen in hypersensitivity pneumonitis.

On epidemiologic grounds, respirable particles from chilled-water air-conditioning systems in textile production plants have been implicated as a cause of hypersensitivity pneumonitis. We have purified the antigen from scum growing in this chilled water by antibody-affinity chromatography by use of IgG isolated from a pool of serum obtained from three workers with disease. Two patients with the disease, three coworkers without the disease, and two unexposed control subjects inhaled a dose of the purified antigen approximately equivalent to that amount calculated to be inhaled during an 8-hour work shift. Both workers with disease experienced fever, malaise, cough, and dyspnea 6 to 8 hours after the aerosol challenge. In these two patients the exposure evoked a transient decrease in circulating lymphocytes, predominantly T cells. Before challenge the patients' peripheral blood mononuclear cells demonstrated a blastogenic response to the antigen. The responding cells had disappeared from the circulation 24 hours after the challenge. Seventy-two hours after the challenge, mononuclear cells that were producing large amounts of specific IgG antibody appeared in the circulation. We conclude that the same antigen(s) that react with IgG antibody produced an acute episode of the disease, that specific antigen-recognition cells disappear from the peripheral blood after exposure to the antigen (presumably because they are attracted to the lung), and that antibody-forming cells appear in the peripheral blood approximately 2 days after a challenge. These antigen-specific reactions of circulating mononuclear cells may be specific for the disease, but studies on a larger number of cases are needed to be certain.

Aerosols↗
PubMed1986

Airway responses to inhaled ouabain in subjects with and without asthma.

Challenges with ouabain and histamine were performed a week apart in 10 patients with asthma and 5 normal subjects. Concentrations were increased cumulatively until specific airway conductance decreased by 30% or the maximal concentration of 1.0% was reached. At low concentrations, ouabain induced bronchodilatation in six patients who had asthma. Bronchodilatation gradually decreased with increasing concentrations and was followed by bronchoconstriction in two patients with asthma who had high airway sensitivity to histamine. Ouabain caused only bronchoconstriction in three patients with severe asthma. The normal subjects showed mild bronchodilatation or no response to ouabain. Several possible biochemical mechanisms may be responsible for the bronchodilatory response to low doses of ouabain, such as stimulation of adenylate cyclase or (Na+,K+)-adenosine triphosphatase. The absence of a bronchodilatory response to ouabain in patients with severe asthma suggests an impairment in the activity of these enzymes.

Adult↗
PubMed1986

Airway responses to inhaled ouabain and histamine in conscious guinea pigs.

Tracheal Na+-K+-ATPase activity is positively correlated with in vivo airway responsiveness to histamine. We wondered whether this were a chance association or whether it was directly related to the mechanism of hyperreactivity. Therefore, we obtained dose-response curves to aerosols of histamine and ouabain in guinea pigs to determine whether an in vivo relationship existed between the excitatory effects of histamine and the enzyme-inhibiting effect of ouabain. Airway responsiveness to ouabain was measured as the ouabain concentration producing a 30% decrease in specific airway conductance (ED30) or that producing a half-maximal response (ED50). Responsiveness to histamine was measured either as ED30 or as ED50. Significant positive correlations were noted between the log ED50 of ouabain and log histamine ED30 or ED50 (r = 0.81 and 0.83, respectively; P less than 0.001), and between log ouabain ED30 and log histamine ED30 and ED50 (r = 0.76 and 0.77, respectively; P less than 0.002). Pretreatment with ouabain increased airway responsiveness to histamine (P less than 0.05). We suggest that in hyperreactive airways Na+-K+-ATPase serves a homeostatic function of preventing Na+ and Ca2+ loading of the cell and that it is not directly responsible for the hyperreactivity.

Aerosols↗
PubMed1986

Effect of heart weight on distribution of lung surface pressures in vertical dogs.

In head-up dogs the vertical gradient of transpulmonary pressure (VGTP) disappears after pneumothorax develops. Our laboratory recently confirmed that the heart moves downward and posteriorly with pneumothorax. To study the extent to which the heart is supported by the lungs, we used a linear elasticity model and finite-element analysis. The lung and heart were assumed to be symmetric along a vertical axis. Reported values of the elastic properties of lung and heart were assigned. The model was generated first without the heart, using the lung alone. The heart was then added to the model. Finally, heart weight was doubled. Adding the heart caused the VGTP to increase; doubling the heart weight further increased the VGTP. These increases were more pronounced at higher lung volumes. Lung inflation was accompanied by an upward displacement of the heart. Inclusion of the heart caused increased inhomogeneities in regional volume distribution. The effect of heart weight may in part explain why the VGTP in the head-up dog is greater than that predicted by lung density.

Animals↗
PubMed1986

Simulation of the vertical gradient of transpulmonary pressure by stable foams.

We describe a simulation of the vertical gradient of transpulmonary pressure (VGTP) using a stable foam, which is suitable for use in studies of the effect of the VGTP on excised lungs. We generated foams that produced linear hydrostatic pressure gradients (HPGs) from 0.18 to 0.44 cmH2O/cm depth, which were stable over time and were reproducible. The HPG was similar under static and dynamic conditions. The foam did not affect lung elastic properties or cause histological changes. We conclude that these stable foams provide a practical, inexpensive simulation of the VGTP and should be useful in studying the effects of the VGTP on regional lung behavior.

Animals↗
PubMed1986

A canine model of bronchial injury induced by nitric acid. Lung mechanics and morphologic features.

We created a model of airway obstruction that avoids long-term toxic exposure. Bronchial injury was induced in 7 dogs by exposure to nebulized 1% nitric acid (HNO3) on alternate days for 4 wk. Lung mechanics were measured prior to exposure and after 2 and 4 wk. Both TLC and VC decreased and the FRC/TLC ratio increased. Expiratory flows decreased while breathing air and an 80% helium-20% oxygen mixture; the volume of isoflow increased. Pulmonary resistance increased and dynamic compliance decreased. On single-breath nitrogen washout, there were increases in the slope of phase III and in closing capacity. Histologically, there was widespread chronic airway inflammation, slight epithelial changes, slight peribronchiolar fibrosis, and an increase in smooth muscle. Pathologic scores were significantly higher in the HNO3-exposed group than in the control group. Scores for peripheral and central airway pathology were correlated with results of tests of airway obstruction.

Airway Resistance↗
PubMed1986

Pulmonary function in relapsing polychondritis.

The pulmonary mechanics and bronchoscopic findings in 5 patients with relapsing polychondritis were studied to evaluate the mechanism of obstruction. Two of the patients did not have clinical symptoms referable to the respiratory tract: pulmonary function was normal in 1 patient and was suggestive of mild restriction in the other. Three patients had dyspnea; pulmonary function studies revealed expiratory and inspiratory obstruction in all 3. The maximal flow-static recoil curves demonstrated that the expiratory obstruction was due predominantly to airway abnormality and not to loss of elastic recoil forces of the lung. The bronchoscopic appearance of the extrathoracic airway during quiet breathing did not accurately reflect pulmonary function results. One patient had a visually normal upper airway but greatly reduced maximal inspiratory flow rates, whereas another patient had pronounced narrowing of the upper airway but only a modest reduction of maximal inspiratory flow rates. The bronchoscopic appearance of the intrathoracic airway during quiet breathing did relate well to maximal expiratory flow rates. We conclude that in our group of patients the predominant mechanism of expiratory obstruction in relapsing polychondritis is due to airway abnormality. Although the bronchoscopic and radiographic findings are useful, spirometry is more important in determining functional abnormality.

Adrenal Cortex Hormones↗
PubMed1985

Influence of the heart on the vertical gradient of transpulmonary pressure in dogs.

Estimations were made of the vertical gradient of transpulmonary pressure (VGTP) from measurements of esophageal pressure in nine head-up dogs at functional residual capacity (FRC) when alive, when dead, and after total bilateral pneumothorax. The VGTP of 0.4 cmH2O/cm height in the alive state was abolished by pneumothorax, and roentgenograms showed that the heart moved in a caudal-dorsal direction. There was a small but significant increase in the VGTP on going from FRC to near total lung capacity (TLC) in alive head-up dogs. In eight dead head-up dogs heart weight was increased by replacing various amounts of heart blood with Hg. The VGTP was significantly increased from 0.28 to 0.51 cmH2O/cm height. The fractional increase in the VGTP was similar to the fractional increase in heart weight. In five dogs extrapolation to zero heart weight gave an average VGTP of 0.14 cmH2O/cm height. We conclude that the lungs help support the heart in the head-up dog and that the VGTP is in part determined by the pressure distribution required for this support.

Animals↗
PubMed1985

Interdependence of regional expiratory flow.

Flows from different lung regions interact at the junctions of the bronchial tree, and flow from each region depends on the driving pressures for other regions. At each junction, flow from the region with the higher driving pressure is favored. As a result there is a limit on the difference in alveolar pressures that can develop during expiratory flow from a lung with regional differences in lung compliance and airway resistance. The limiting pressure difference is smaller for lower flow. A nonuniform lung therefore empties more uniformly if it empties slowly, and maximum flow at low lung volume may be greater than it would be at the same lung volume during a maximal expiratory vital capacity maneuver.

Airway Resistance↗
PubMed1984

Induction of nasal late-phase reactions by insufflation of ragweed-pollen extract.

We studied changes in NAC in 17 ragweed-sensitive individuals after intranasal ragweed-challenge testing. All patients experienced immediate symptoms of sneezing, rhinorrhea, and nasal congestion that were associated with marked decreases in NAC (mean = 68%). In 10 trials patients also experienced late (greater than 0 hr) symptoms of nasal congestion with or without rhinorrhea; the mean late NAC decrease in this group was 42%. In contrast, no late symptoms were noted in nine trials, and the mean NAC decreased 5% in this group (p less than 0.003). Attempts to passively transfer immediate or late nasal sensitivity to one individual by spraying the nasal cavity with IgE antibody-containing serum, by packing the nose with cotton pledgets soaked in serum, by injecting serum directly into the inferior turbinate, and by transfusion with IgE-containing serum were not successful. We conclude that symptomatic late-phase reactions occur in the nose after intranasal challenge in about 50% of patients and that these symptomatic reactions can be confirmed objectively by rhinomanometry.

Adult↗
PubMed1984

Quiet-breathing vs. panting methods for determination of specific airway conductance.

Specific airway conductance (sGaw) was measured during quiet breathing and during panting in 21 normal subjects and 10 patients with obstructive lung disease. The direct method used does not require measuring thoracic gas volume (TGV). Coefficients of variation were 5.5% for panting and 5.1% for quiet breathing. Interobserver variability was 4.7% in the quiet-breathing method and 6.3% in the panting method. The two methods gave equivalent results for sGaw. A slightly greater sGaw was found by the panting method in normal subjects with the highest sGaw values, probably due to widening of the oropharynx-glottis during panting. In six normal subjects studied for intrasubject variability over time, no significant diurnal or day-to-day variability was seen by either method. We conclude that the quiet-breathing method is a simple valid means of determining sGaw and utilizes a physiological respiratory maneuver. Obviation of the need to measure TGV is advantageous. Results are equivalent to those of the panting method and variability is similar.

Adult↗
PubMed1983

Effect of left pneumonectomy on lung mechanics in rabbits.

Left pneumonectomy was performed in nine rabbits at 10 wk of age. Detailed pulmonary mechanics studies were performed at 14 wk of age in these rabbits and in nine littermate controls. Lung weight, total lung capacity, and static lung pressure-volume curves of the pneumonectomized rabbits were not different from those of the controls, but the forced vital capacity was smaller (P less than 0.05). Tantalum bronchograms of excised right lungs revealed no difference between controls and pneumonectomized rabbits in terms of bronchial diameter or pressure-area behavior of central or peripheral airways. Airways of pneumonectomized rabbits lengthened in accordance with the increase in lung volume. Over the midvolume range, the flow-limiting site moved from the trachea in controls to the right main bronchus in pneumonectomized rabbits. Maximal expiratory flow on air and on 80% He-20% O2 in the pneumonectomized rabbits average 70% of that in controls. This difference in flow was consistent with predictions based on the wave-speed theory of flow limitation.

Animals↗
PubMed1983

Expiratory flow limitation.

The first major advance in understanding expiratory flow limitation of the lungs came with the description of isovolume pressure-flow curves. These curves documented the existence of a volume-dependent limit to maximal expiratory flow and led directly to the description of the maximal expiratory flow-volume (MEFV) curve. Definitive modeling of flow limitation awaited the description of a localized mechanism that dominated the flow-limiting process. The phenomenon of wave speed limitation of flow was shown to apply to the airways and provided the needed localized mechanism. Using this concept and recent data on airway mechanics and the frictional losses in the flow, a computational model of the MEFV curve has been developed. Further progress will require modeling of inhomogeneous emptying in diseased lungs, perfecting noninvasive techniques of estimating pertinent airway characteristics, and improving techniques for increasing the signal-to-noise ratio in MEFV curves.

Forced Expiratory Flow Rates↗