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Biomedical subjects

M A Sackner

Publications and source records attributed to M A Sackner.

At least 91 records · Page 5Linked to original sources
PubMed1982

Response to bronchodilator drug administration by a new reservoir aerosol delivery system and a review of other auxiliary delivery systems.

Response to bronchodilator aerosols delivered by metered dose inhalers (MDI) depends in part upon the amount of drug depositing on the airways. Ideally, the MDI should be actuated during a slow deep inhalation followed by a breathholding pause, an impossible maneuver for many patients. We developed a new reservoir aerosol delivery system (RADS) consisting of a 700-ml collapsible bag in which aerosol could be injected. The mouthpiece-canister was filtered with a reed that vibrated at inspiratory flows greater than 0.3 L/s to produce a noise. Patients were instructed to keep inhalation silent while breathing from RADS. One puff of metaproterenol (650 microgram) administered via RADS (with one breath rebreathed) was compared with one puff of metaproterenol (650 micrograms) from usual MDI using serial measurements of body plethysmography and spirometry. Respiratory inductive plethysmography measured the point of MDI actuation, volume of inhalation, inspiratory flow, and breathholding pause. Ten patients with chronic airflow limitation caused by asthma or chronic bronchitis were given typed instructions on MDI usage and trained shortly before the study. Metaproterenol via RADS produced significantly greater maximal increase in SGaw (195 +/- 52% SE) compared with metaproterenol via conventional MDI (101 +/- 24%, p less than 0.003). Bronchodilator response in 4 patients unable to coordinate actuation of the MDI with inspiration was significantly less than in 6 patients with good MDI technique (p less than 0.005). The mean flow rates were 0.54 +/- 0.16 L/s during inhalation of metaproterenol compared with 0.19 +/- 0.02 L/s and 0.24 +/- 0.03 L/s during the first and second inhalations, respectively, using RADS. This reservoir aerosol delivery system, which was well accepted by the patients, promotes more effective bronchodilation than the conventional metered dose inhaler.

Adult↗
PubMed1982

Assessment of density dependent flow-volume parameters in nonsmokers and smokers. Measurement with spirometry, body plethysmography and respiratory inductive plethysmography.

The purpose of this investigation was to assess the density-dependent flow-volume components of the forced vital capacity using simultaneous spirometry, respiratory inductive plethysmography, and body plethysmography in the detection of small airway disease. The forced vital capacity was measured during air, helium-oxygen and sulfur-hexafluoride breathing to provide a range of gas density influences. Combining flow measured at the mouth with volume referenced to change in alveolar gas volume as measured by body or respiratory inductive plethysmography during helium-oxygen breathing accentuated the differences between nonsmokers and smokers because of the variable degree of alveolar gas compression occurring over the second half of FVC. The volume of isoflow obtained when comparing the helium and oxygen mixture to air also effectively separated nonsmokers from smokers. The utilization of the high density gas mixture, sulfur hexafluoride-oxygen during the FVC maneuver did not provide useful diagnostic information. Therefore, density-dependent flow-volume information using helium as a test gas alone or compared to air with a variety of analyses is a good approach to detection of early lung disease in smokers.

Adolescent↗
PubMed1982

Assessment of time-volume and flow-volume components of forced vital capacity. Measurement with spirometry, body plethysmography and respiratory inductive plethysmography in nonsmokers and smokers.

The purpose of this investigation was to assess the effectiveness of the time-volume and flow-volume components of the forced vital capacity measured by simultaneous spirometry, respiratory inductive plethysmography, and body plethysmography in detecting small airway disease. Spirometry measured the exit of gas from the lungs, whereas body plethysmography measured both the exit of gas and alveolar gas compression. Respiratory inductive plethysmography, which reflected change in thoracic volume, provided semi-quantitative data f both gas exit and alveolar gas compression which generally lay between spirometry and body plethysmography. In nine nonsmokers and 12 smokers (six with small airway disease as defined by abnormal closing volumes and alveolar uniformity), analysis of forced vital capacity revealed that the only test which differentiated nonsmokers from smokers was the higher spirometric estimation of maximum expiratory flow measured at 25 percent VC in nonsmokers. Combining flow measure at the mouth with volume referenced to change in alveolar gas volume as measured by body or respiratory inductive plethysmography did not differentiate nonsmokers from smokers. Moment analysis performed of forced vital capacity with all of the three devices did not distinguish nonsmokers from smokers. The data in this study and a review of other investigations indicate that the time-volume and flow-volume components of the forced vital capacity on air breathing are not very sensitive in detecting early lung disease in smokers.

Adolescent↗
PubMed1982

Subjective and objective measurement of cigarette smoke inhalation.

The pattern of cigarette smoke inhalation was studied in 19 smokers with respiratory inductive plethysmography, a reliable unobtrusive ventilatory monitoring device. The mean volumes inhaled varied widely from 0.27 to 1.97 L, with a group mean (+/- SD) of 0.79 +/- 0.45 L. Mean duration of smoke inhalation varied from 2.0 to 6.8 seconds, with a group mean of 4.5 +/- 1.3 seconds. An inhalation fraction was derived by dividing the inhaled volume by the vital capacity; this fraction varied from 0.09 to 0.47, with a group mean of 0.20 +/- 0.10. Subjects rated the depth that they inhaled smoke into their lungs on a visual analog scale and on a grading system. Correlation between visual analog scale and inhalation fraction was poor (r = -0.15). Also, inhalation fraction bore no relationship to smoking pack-years or current pulmonary function. The smokers' inaccurate assessment of their inhalation pattern may help to explain the poor correlation reported between cigarette smoke inhalation and severity of obstructive lung disease.

Adult↗
PubMed1981

Effects of brief and intermediate exposures to sulfate submicron aerosols and sulfate injections and cardiopulmonary function of dogs and tracheal mucous velocity of sheep.

Pulmonary mechanics of anesthetized dogs were not changed or were minimally altered by breathing the following compounds as submicron aerosols in concentrations up to 17.3 mg/m3 for 7.5 min: (1) sodium chloride (as a control), (2) sodium sulfate, (3) ammonium sulfate, (4) zinc sulfate, (5) zinc ammonium sulfate, (6) ammonium bisulfate, (7) aluminum sulfate, (8) manganese sulfate, (9) nickel sulfate, (10) copper sulfate, (11) ferrous sulfate, and (12) ferric sulfate. Submicron aerosols of these compounds in concentrations of 4.1-8.8 mg/m3, administered for 4 h to anesthetized dogs, did not affect mechanics of breathing, hemodynamics, and arterial blood gases. In conscious sheep, tracheal mucous velocity was not altered by exposure to the submicron aerosols of the sulfate compounds. None of these compounds, injected iv in a dose of 1 mg, had adverse effects on mechanics of breathing, pulmonary and systemic hemodynamics, or arterial blood gases. In 100-mg injections, zinc sulfate and zinc ammonium sulfate produced a fall in cardiac output, systemic hypotension, hypoxemia, and metabolic acidosis. Copper sulfate at this dose produced pulmonary hypertension, a fall in cardiac output, hypoxemia, respiratory acidosis, and a decrease of specific total respiratory conductance. It is concluded that submicron aerosols of sulfate salts do not have adverse cardiopulmonary effects when administered in high concentrations for up to 4 h. However, prolonged exposure to high concentrations of zinc sulfate, zinc ammonium sulfate, and copper sulfate aerosols should be carefully monitored because of the possibility that lower levels of these compounds in the bloodstream for long time period might have adverse cardiopulmonary effects.

Aerosols↗
PubMed1981

Acute pulmonary hemodynamic effects of intravenous copper sulfate: role of alpha-adrenergic system.

We investigated the acute pulmonary hemodynamic effects of intravenous copper sulfate (CuSO4) infusion and its mechanism of action in six groups of conscious sheep (total 40). After 300 mg CuSO4 alone, mean pulmonary artery pressure (Ppa) increased from 10.3 to 22.5 Torr and pulmonary artery wedge pressure (Ppaw) from 3.5 to 7.6 Torr, whereas systemic arterial pressure (Psa) increased from 95 to 102 Torr. Cardiac output (Qp) decreased from 4.7 to 3.3 l/min. Pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) increased to 320 and 160% of base line, respectively. The hemodynamic changes correlated well with serum copper, which increased from a base-line value of 0.12 to 3.5 mg/dl after the CuSO4. Serum dopamine beta-hydroxylase increased from 3.2 U/l before CuSO4 injection to 5.7 after its administration, signifying activation of adrenergic nervous system. H1-histamine receptor blockade with chlorpheniramine failed to prevent the effects of CuSO4. Pretreatment with methysergide, a serotonin antagonist, partially attenuated the effects of CuSO4. Phenoxybenzamine, an alpha-adrenergic receptor blocker, and 6-hydroxydopamine, a catecholamine depleting agent, completely blocked the effects of CuSO4. beta-Adrenergic receptor blockade with propranolol enhanced the effects of CuSO4. We conclude, that, in conscious sheep, acute infusion of CuSO4 caused a marked reversible increase in PVR with a slight transient increase in SVR, and this pulmonary hypertension was produced by stimulation of the alpha-adrenergic nervous system.

Animals↗
PubMed1981

Differences in airway reactivity in normal and allergic sheep after exposure to sulfur dioxide.

The effect of breathing 5 ppm sulfur dioxide (SO2) on airway reactivity was studied in both normal and allergic conscious sheep. Allergic sheep were defined as animals in which inhalation of Ascaris suum extract resulted in bronchospasm as evidenced by an increase in mean pulmonary flow resistance (RL), hyperinflation, and a fall in dynamic compliance. Airway reactivity was assessed by measuring the increase of RL after 18 breaths of 0.25% carbachol (c), from an initial RL value obtained after 18 breaths of buffered saline (s) [RL(c-s)]. RL and RL(c-s) were determined prior to, immediately after, and 24 h after exposure to 5 ppm SO4 for 4 h. In both groups RL remained unchanged after SO2 exposure. Prior to exposure, RL(c-s) was not significantly different in seven normal (0.3 +/- 0.1) and seven allergic sheep [0.4 +/- 0.2 (SD) cmH2O X l-1 X s], and there was no significant change in RL (c-s) immediately after SO2 exposure in either group. Twenty-four h later, RL(c-s) RL(c-s) increased to 0.7 +/- 0.8 (P less than 0.2) in normal and to 1.8 +/- 0.9 cmH2O X l-1 X s (P less than 0.01) in allergic sheep. Because the increase in RL(c-s) after 24 h was greater (P less than 0.01) in allergic than in normal sheep, we conclude that SO2 exposure increased airway reactivity more in the former than in the latter.

Animals↗
PubMed1981

Noninvasive ventilatory monitoring by respiratory inductive plethysmography in conscious sheep.

The respiratory inductive plethysmograph is a noninvasive device that has been used to measure tidal volume (VT) in humans from changes in self-inductance of wire coils excited by an oscillator circuit placed about the rib cage and abdomen. We investigated its accuracy in conscious sheep utilizing a new calibration procedure during quiet breathing and breathing associated with bronchospasm provoked by aerosolized carbachol. Seven sheep were intubated with a nasotracheal tube and an esophageal balloon placed for determination of transpulmonary pressure. Base-line mean pulmonary flow resistance (RL) in the sheep was 1.5 +/- 0.7 (SD) cmH2O X l-1 X s. After carbachol inhalation, mean RL increased to a maximum of 8.8 +/- 2.8 cmH2O X l-1 X s (P less than 0.002). AT base line, mean VT estimated by respiratory inductive plethysmography over a 20-s period fell within +/- 6% of spirometry. After carbachol VT in five of the sheep remained close to the initial validation, but in two, it deviated +/- 11% from spirometry. Analysis of the continuous recording of timing and volume components of the breaths revealed that bronchoprovocation did not significantly alter mean VT or frequency. However, there was a slight increase in both parameters resulting in an increase in minute ventilation from 7.6 +/- 2.4 to 9.6 +/- 2.8 l/min (P less than 0.02). Similarly, a slight decline in inspiratory time coupled with the slight rise in VT produced an increase in mean respiratory flow from a base-line value of 0.35 +/- 0.12 to 0.44 +/- 0.17 l/s (P less than 0.05). These results indicate that the respiratory inductive plethysmography accurately monitors breathing pattern in conscious sheep even during severe bronchospasm.

Animals↗
PubMed1980

Sulfur dioxide induced airway hyperreactivity in allergic sheep.

The effects of a four-hour exposure (via a Plexiglas hood) to sulfur dioxide (SO2) on airway reactivity was studied in both normal and allergic conscious sheep. Allergic sheep were defined as animals in whom inhalation of Ascaris suum extract resulted in an increase in mean pulmonary flow resistance (RL). Airway reactivity (delta RL) was assessed by measuring the increase in RL after 18 breaths of 0.25% carbachol, from an initial value obtained after 18 breaths of buffered saline. RL and delta RL were determined prior to, immediately after and 24 hours following SO2 exposure in three groups of sheep: six normal sheep exposed to 5 ppm SO2 (group A); six normal sheep exposed to 10 ppm SO2 (group B) and seven allergic sheep exposed to 5 ppm SO2 (group C). RL was not affected by SO2 exposure in any group but both groups B and C showed increases in delta RL 24 hours after exposure. Since the increase in delta RL was greater in group C than in either groups A or B, we conclude that allergic sheep have enhanced susceptibility to the injurious airway effects of SO2.

Airway Resistance↗
PubMed1980

Deposition of ragweed pollen and extract on nasal mucosa of patients with allergic rhinitis: effect on nasal airflow resistance and nasal mucus velocity.

This study was undertaken to ascertain whether nasal mucus velocity (NMV) could be altered by short-term exposure to antigen. Asymptomatic patients with a history of allergic rhinitis who had a positive cutaneous reaction to ragweed extract were investigated. The plan was to achieve approximately a fourfold elevation of nasal airflow resistance (NAR) with antigen challenge and then obtain serial measurements of NAR and NMV. NMV was not significantly altered when the antigen was introduced by nasal inhalation of (1) ragweed pollen grains, (2) nebulized ragweed extract for 10 breaths, and (3) nebulized ragweed extract for 30 min on each of 3 successive days. When ragweed extract was introduced by direct instillation of the solution into the nose, NMV fell below baseline values at either 0.5 or 1.5 hr, or at both times after administration. Persistence of impairment of mucociliary transport at a time when nasal airway constrictor response had dissipated suggested that a chemical mediator might have been responsible for the alteration of clearance. The failure to demonstrate depression of mucus transport with the inhalation studies might have been due to insensitivity of the radiopaque Teflon disk method or to a qualitatively different allergic reaction to direct instillation of antigen solution.

Adult↗
PubMed1980

Sensitivity of bronchoprovocation and tracheal mucous velocity in detecting airway responses to O3.

This study was undertaken to determine whether measurements of tracheal mucous velocity or airway reactivity to inhaled carbachol more sensitively detect airway effects of inhaled ozone (O3) in conscious sheep. Dose-response curves of mean pulmonary flow resistance (RL) to carbachol were obtained by measuring RL after five breaths of carbachol aerosol with stepwise increases in drug concentration. The animals then breathed 0.5 ppm O3 through an endotracheal tube for 2 h. The dose-response curves were repeated immediately after the 0.5 ppm O3 exposure and 24 h later. In the eight sheep studied, there were no significant alterations in base-line RL immediately after or 24 h after 0.5 ppm O3. Airway hyperreactivity was not apparent immediately after the sheep breathed 0.5 ppm O3, but it was evident 24 h later. In contrast, six sheep that breathed 0.5 ppm O3 in the same manner for 2 h did not show a significant depression in tracheal mucous velocity the same day or 24 h later. Exposure to 1 ppm O3 for 2 h resulted in airway hyperreactivity immediately after the exposure and elevated base-line RL 24 h later; 2 ppm O3 produced an increase in base-line RL immediately after exposure. We conclude that, in conscious sheep, airway hyperreactivity appears to be a more sensitive indicator of airway effects produced by short-term exposure to 0.5 ppm O3 than depression of tracheal mucous velocity.

Airway Resistance↗
PubMed1980

Rebreathing techniques for pulmonary capillary blood flow and tissue volume.

The variability of three methods of calculating pulmonary capillary blood flow (Qc) and pulmonary tissue plus capillary blood volume (Vt) during rebreathing was assessed in normal humans by using as markers acetylene, ethyl iodide, and dimethyl ether. The methods of analysis were as follows. Method I, the timing of the disappearance curves of the soluble gases was corrected by assuming that the C18O-disappearance curve intercepted at unity at time O. Method II, it was assumed that the acetylene Qc calculated by method I was correct; ethyl iodide and dimethyl ether Vt were solved by an equation using the disappearance slopes of these gases and the acetylene Qc value, thereby avoiding dependence on extrapolated intercept values. Method III, Vt was calculated by solving for a unique value of Qc between pairs of disappearance slopes of acetylene and dimethyl ether, acetylene and ethyl iodide, and ethyl iodide and dimethyl ether. Among the three methods, method I gave the most reproducible values for Vt as determined with acetylene or dimethyl ether. Using method I, both acetylene and dimethyl ether were equally acceptable gases for measurement of Vt; acetylene was a better marker for Qc measurements.

Adult↗
PubMed1980

Non-invasive measurement of ventilation during exercise using a respiratory inductive plethysmograph. I.

The respiratory inductive plethysmograph, a monitor of ventilation that does not require a connection from the airway, was validated against spirometry during moderate exercise using a bicycle ergometer and a treadmill. One hundred seventy-three of 200 breaths during bicycle exercise from 6 young adults and 211 of 242 breaths during treadmill walking were within +/- 20% of the tidal volumes measured by simultaneous spirometry. The respiratory inductive plethysmograph appears to be a useful non-invasive monitor of ventilation during exercise.

Adolescent↗
PubMed1980

Effects of breathing through external dead space on ventilation at rest and during exercise. II.

We used a new non-invasive monitor of ventilation, the respiratory inductive plethysmograph, to determine the effects of breathing through a mouthpiece (with nose clip) and breathing through external dead spaces on ventilation at rest and during exercise. Six normal young subjects were studied during 5-min sequential periods at rest, submaximal exercise on a bicycle at a work load of 800 kgm/min, and recovery. Not surprisingly, the imposition on the respiratory system of breathing through a mouthpiece (with nose clip) and with external dead spaces of 150, 250, and 350 ml produced progressively greater ventilation than natural breathing during rest and submaximal bicycle exercise. However, when the actual tidal volumes were corrected for the increase in ventilation caused by the external dead space, ventilation both at rest and during exercise with mouthpiece breathing still remained higher than natural breathing. These data suggest that breathing through a mouthpiece (with nose clip) and breathing through external dead spaces stimulates ventilation both at rest and during exercise.

Adult↗