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Biomedical subjects

R H Ingram

Publications and source records attributed to R H Ingram.

At least 73 records · Page 4Linked to original sources
PubMed1983

Density dependence of maximal flow in dogs with central and peripheral obstruction.

In 12 anesthetized, tracheotomized, vagotomized, open-chested, mongrel dogs we measured end and side hole airway pressures during forced expiration using a Pitot static probe. Volume was obtained as the integral of flow from a dog plethysmograph with frequency response adequate to 20 Hz. Equal pressure points (EPPs) and choke points (CPs) were located with dogs breathing air or a mixture of 80% helium-20% oxygen (HeO2) before and after partial obstruction of the trachea and intravenous histamine and propranolol. At 50% of vital capacity (VC) the CP was in the trachea in 11 of 12 dogs. Partial obstruction of the trachea decreased flow during the plateau of the maximum expiratory flow-volume curve (MEFVC) with the CP remaining in the trachea. The MEFVC plateau was extended to a lower lung volume. At 50% of VC the EPP moved downstream and density dependence remained high. Histamine and propranolol caused EPPs and CPs to move towards the periphery and density dependence to decrease. The shape of the MEFVC changed as the plateau was shortened and, in some instances, abolished. A plateau on the MEFVC could be regenerated by partial obstruction of the trachea. This was accompanied by return of the CP to the trachea and an increase in density dependence. Changes in density dependence were found to be a result of both the relocation of sites of flow limitation and differences in local CP areas with HeO2 and air.

Airway Obstruction↗
PubMed1983

Effect of intermittent mandatory ventilation on respiratory drive and timing.

Seven patients receiving chronic ventilatory support were studied to better define the effects of intermittent mandatory ventilation (IMV) on the control and timing of spontaneous breathing between mandatory breaths. Each of these patients could sustain adequate spontaneous ventilation, as reflected by stable end-tidal carbon dioxide concentration (FETCO2), and arterial oxygen saturation (SO2) during periods of unassisted ventilation of sufficient duration to allow study. Inspiratory time (TI), respiratory cycle duration (Ttot), tidal volume (VT), and tracheal occlusion pressure (P0.1) were measured as IMV rate was progressively reduced. Respiratory timing was unaltered by decreasing IMV frequency; however, VT increased progressively. The P0.1 and mean inspiratory flow rate (VT/TI) also increased with each decrease in IMV rate, whereas FETCO2 and arterial SO2 remained constant. Thus, in these stable but ventilator-dependent patients, IMV did not alter respiratory timing or chemical stimuli, but it did alter respiratory drive as measured by VT/TI and P0.1.

Adult↗
PubMed1983

Chest wall configurational changes before and during acute obstructive episodes in asthma.

We induced bronchial obstruction in 7 otherwise healthy asthmatic subjects and then measured the degree of airway obstruction and the dimensions of the chest wall including the anteroposterior (AP) diameters of the upper and lower rib cage and the abdomen and the transverse diameter of the lower rib cage. Airway obstruction was accompanied by a pronounced increase in the end-expiratory AP diameter of the upper rib cage in all 7 subjects and of the low lateral rib cage in 3 of the 4 subjects in whom this was measured. Other end-expiratory dimensions showed variable changes. In 6 of 7 subjects, obstruction caused the lower rib cage to become more elliptical in cross section during inspiration; transient inward motion of the lower anterior rib cage during early inspiration was noted. This latter motion coupled with the continuous outward motion of the upper anterior rib cage produced a pronounced rocking motion of the sternum during inspiration. These distortions of the chest cage were maximal when obstruction was most severe and gradually diminished as obstruction resolved. These inspiratory changes in chest cage cross-sectional configuration are similar to those seen in normal subjects who attempt to overcome external resistive loading by the increased use of inspiratory muscles; the end-expiratory configuration in asthma indicates an increase in functional residual capacity, which is actively maintained. Multiple degrees of freedom of motion of the chest cage exist during obstructive episodes. Estimates of volume change from measurements of rib cage cross-sectional area and abdominal diameter should be made with caution.

Abdomen↗
PubMed1983

Are exercise and isocapnic voluntary hyperventilation identical bronchial provocations?

There is a positive and direct relationship between the magnitude of heat lost from the respiratory tract, the degree of cooling of intrathoracic airways and the magnitude of the airway obstructive response that develops in asthmatic subjects following exercise. We explore the possibilities of the causal nature of this relationship, the potential mechanisms by which they may relate and attempt to focus on the controversies that still exist with regard to the equivalency of respiratory heat loss (RHL) produced by exercise and by isocapnic voluntary hyperventilation (VHV) in asthmatics.

Asthma↗
PubMed1982

Airway cooling in asthmatic and nonasthmatic subjects during nasal and oral breathing.

It has been suggested that nasal breathing attenuates the airway obstruction that follows physical exertion in asthmatics. In an effort to determine the reason for this protection, we had nine asymptomatic asthmatics and five normal subjects inhale subfreezing air at equal ventilations through either their noses or mouths in a random fashion while we measured the temperature in the retrotracheal esophagus (Trt). Pulmonary mechanics recorded before and after voluntary eucapnic hyperventilation simulating moderately heavy workloads demonstrated a mean fall in forced expiratory volume in one second (as a representative variable) of 28.6% +/- 4.8% (SEM) and 7.5% +/- 1.9% from control in the oral and nasal challenges, respectively, in the asthmatic subjects (p less than 0.001). Measurement of Trt during hyperventilation showed a mean fall of 2.7 degrees +/- 0.05 degree C with nasal breathing in this group (p less than 0.0001) and a linear relationship between the degree of airway cooling and the severity of subsequent bronchoconstriction (r=0.81). The normal subject showed similar changes in temperature but did not change their lung function. These data demonstrate that nasal ventilation minimizes airway cooling in both normal and asthmatic individuals through more efficient conditioning of inspired air, and it is through this mechanism that this form of respiration protects against exercise-induced bronchospasm.

Adult↗
PubMed1982

Controlled-analysis of the effects of inhaled lignocaine in exercise-induced asthma.

To determine whether anaesthesia of the intrathoracic airways would attenuate the development of exercise-induced asthma, we studied eight symptomless asthmatic patients by cycle ergometry after saline or lignocaine pretreatment while they were breathing air at 24 degrees C with 9.1 mg of H2O/l. Pulmonary mechanics were measured before and after the administration of each agent, and again five minutes after cessation of exercise. Sufficient lignocaine was administered to abolish the gag reflex and the cough response to aerosols of citric acid. Before exercise there were no significant differences for any lung function variable between the saline and lignocaine results. Equally, there were no significant differences between these agents for minute ventilation (VE) during exercise (VE lignocaine = 71.0 +/- 7.4 (SEM) l/min; VE saline 67.2 +/- 8.1 l/min;), or in the severity of the subsequent bronchospastic response (for example, the FEV1 with saline was 22.6 +/- 2.9% decrease, and with lignocaine 23.6 +/- 8.5%). Thus these results do not support the idea that there are thermally sensitive neural receptors in intrathoracic airways that play a role in the pathogenesis of exercise-induced asthma.

Adult↗
PubMed1982

Bronchodilatation, lung recoil, and density dependence of maximal expiratory flow.

Using normal human subjects we have measured maximal expiratory flow rates with air (Vmaxair) and after a washin of 80% He-20% O2 (VmaxHeO2) and static elastic recoil pressures of the lung [Pst(L)] both before and after administration of a beta-agonist, terbutaline. The effects of inhaled drug were compared with those of the subcutaneously administered agent, each given in doses to produce maximal bronchodilatation as assessed by increases in Vmaxair in the mid-vital capacity. Although there was a significant yet modest decrease in Pst(L) only after injection of the agent, density dependence (DD), assessed as the ratio of VmaxHeO2 to Vmaxair, increased significantly and comparably after either route of administration. A modest decrease in Pst(L), therefore, did not affect the changes in DD.

Adolescent↗
PubMed1982

Effects of inhaled sympathomimetics on obstructive response to respiratory heat loss.

To investigate the influence of inhaled sympathomimetics on the obstructive response to airway cooling, we had six asymptomatic atopic asthmatics perform eucapnic hyperventilation with frigid air at various levels of ventilation after pretreatment with aerosols of metaproterenol or placebo in a random blind fashion. In control experiments, eucapnic hyperventilation produced a progressive decrease in 1-s forced expiratory volume in a stimulus-response fashion as the level of ventilation rose in successive challenges. Metaproterenol did not produce an all-or-none blockade, but rather a parallel shift in the stimulus-response curve so that its protective effects could be overcome by increasing the stimulus. There was no effect on respiratory heat loss. These results explain, in a quantitative fashion, why a treatment schedule that permits a person with asthma to perform a given exercise task without difficulty becomes ineffective as the thermal burden or severity of the task increases.

Adult↗
PubMed1982

Parenteral vs. inhaled atropine: density dependence of maximal expiratory flow.

Using forced vital capacity maneuvers, we measured maximal expiratory flow rates (Vmax) and static elastic recoil pressures of the lung [Pst(L)] using quasi-static maneuvers in normal nonsmoking human subjects who were breathing air and after a washing of 80% helium-20% oxygen before and after both inhaled and intravenously administered atropine sulfate. By both routes there were equivalent increases in Vmaxair but different effects on density dependence (DD) of Vmax (DD = ratio of VmaxHeO2 to Vmaxair) and on Pst(L). At 30% of vital capacity, DD decreased from an average of 1.47 to 1.32 (P less than 0.01, paired t test) after inhaled drug and did not change after parenteral administration [1.44 vs. 1.48 (P greater than 0.2)]. After inhalation Pst(L) did not change, but after parenteral administration Pst(L) significantly decreased. We interpret these findings to indicate a predominantly large-airway effect with the inhalation route and a more uniform dilatation after the parenteral dose. These results contrast with beta-adrenergic dilatation following which small-airway effects predominate regardless of route of administration.

Adult↗
PubMed1982

Density dependence of maximum expiratory flow in the dog.

Airway lateral and impaction pressures were measured during expiratory flow limitation in six anesthetized, vagotomized, tracheally intubated, open-chest dogs with the lungs filled with air or a mixture of 80% helium-20% oxygen (HeO2). Pressures were measured in the vicinity of equal pressure points (EPP) and choke points (CP). Maximum flow (Vmax) was ensured by demonstrating no increase in flow with a 50% increase of driving pressure. At 50% vital capacity, mean density dependence (VmaxHeO2/Vmaxair) was 1.58, which was less than 1.69 predicted for fully density-dependent flow. Transmural pressure and airway area at CP and EPP (located on air) were significantly less with HeO2 than with air. Frictional losses between the alveoli and CP were 40% greater with HeO2 than with air. These enhanced losses were mostly peripheral to the EPP. Frictional loss upstream from the EPP was 47% of the total pressure loss on air and increased to 70% on HeO2. The data at 50% VC suggest that these higher frictional losses with HeO2 resulted in decreased density dependence of Vmax due to different pressure distribution along the airway with a lower transmural pressure and smaller area at the CP.

Air↗
PubMed1982

CO2 elimination by high-frequency oscillations in dogs--effects of histamine infusion.

Effective gas exchange can be achieved in normal dogs by ventilation at frequencies of 4-20 Hz using stroke volumes (SV) smaller than the anatomic dead space. CO2 elimination is largely a function of tracheal SV-frequency product (Vosc) in anesthetized, paralyzed dogs with normal lungs. To determine the effect of constriction of small airways on gas exchange during such high-frequency ventilation (HFV), we ventilated five anesthetized, paralyzed, and vagotomized dogs via a tracheal cannula before and during intravenous histamine infusion. Vosc was varied by varying the frequency while keeping SV constant. For low Vosc, CO2 elimination (VCO2) increased directly with Vosc during control and histamine experiments. At high Vosc, VCO2 continued to increase directly with Vosc during the control study, but during histamine infusion VCO2 was lower than control values. Eucapnia could be maintained in each dog during HFV, even during airway constriction. During histamine infusion the frequency-dependent mechanical properties of the lung influence the delivery of the HFV SV to the respiratory zone, and this may explain the lower VCO2 observed.

Animals↗
PubMed1982

Dose-response effects of atropine on thermal stimulus-response relationships in asthma.

To determine how cholinergic blockade modifies the stimulus-response relationships to thermal provocations, we had seven asthmatics perform increasing levels of eucapnic hyperventilation of subfreezing air (-10.6 +/- 1.9 degrees C) after pretreatment with aerosols of saline and atropine in doses of 0.25, 0.5, 1.0, 3.0, and 6.0 mg. Testing was performed on 5 separate days with both placebo and a single dose of drug. In control experiments, increasing ventilation produced a progressive decrease in the 1-s forced expiratory volume in a stimulus-response fashion. There were no significant differences between any placebo study. Atropine pretreatment did not abolish the obstructive response to airway cooling at any dose but, rather, shifted the stimulus-response curve to the right, so that the effects of muscarinic blockade could be overcome by increasing the stimulus. There were no significant differences between the results observed with 0.25 or 6 mg of atropine. These data demonstrate that cholinergic mechanisms play, at best, a very minor role in exercise-induced bronchospasm and offer a unifying explanation for the disparate findings in the literature regarding antimuscarinic agents in this condition.

Adult↗
PubMed1982

Experimental induction of chronic bronchitis in dogs: effects on airway obstruction and responsiveness.

Chronic bronchitis was induced in 6 mongrel dogs by chronic exposure to SO2 gas; the degree of chronic airway obstruction and the effects on airway responsiveness to inhaled histamine, carbachol, and prostaglandin F2 alpha were examined. Five dogs developed chronic airway obstruction, as indicated by an increase in pulmonary resistance, and clinical mucous hypersecretion. In addition, in each of the animals in which chronic airway obstruction developed there was a decrease in the airway responsiveness to inhaled mediators. Those findings demonstrate that induction of chronic bronchitis in dogs results in hyporesponsiveness to inhaled mediators, a finding distinctly different from that reported in human subjects with naturally occurring disease.

Airway Resistance↗
PubMed1981

Progesterone administration and progressive sleep apneas.

Nine adult patients with obstructive sleep apnea syndrome were administered medroxyprogesterone acetate, 60 to 120 mg/day, and the effect of medroxyprogesterone on clinical symptoms and obstructive apneas during sleep was assessed. Four patients responded with resolution of daytime sleepiness, disappearance of pedal edema, and a decrease in the number of obstructive apneas during sleep. Cessation of therapy led to a return of daytime sleepiness in three and an increase in obstructive apneas in all four subjects. Two responders experienced side effects of alopecia or decreased libido. Before medroxyprogesterone therapy, responders were distinguished from nonresponders only by the presence of a significantly lower resting arterial oxygen tension during wakefulness. We characterize a subgroup of patients who benefit from medroxyprogesterone therapy by reducing obstructive apneas during sleep.

Adult↗
PubMed1981

Effects of beta adrenergic blockade on histamine and prostaglandin-F2 alpha responsiveness in the dog.

To examine whether either the degree of existing beta adrenergic tone or the magnitude of beta adrenergic response during bronchoconstriction might account for the differences that exist between dogs in their pulmonary responsiveness to aerosol challenge with bronchoconstrictor agents, dose-response curves were performed in a group of dogs to either histamine or prostaglandin-F2 alpha, both before beta blockade with propranolol. Beta blocked had no significant effect on control values of dynamic compliance (Cdyn) or resistance of the lung (RL) or on pulmonary responsiveness to prostaglandin f2 alpha. Although propranolol did not have a significant effect on aerosol responsiveness to histamine for the group of dogs taken together, those dogs initially least responsive to aerosol histamine did become more responsive after beta blockade. This effect of beta blockade was statistically significant only for Cdyn and not for RL, suggesting enhancement of peripheral airway effects. We conclude that a beta adrenergic mechanism may contribute to the range of responsiveness found among dogs in their pulmonary responsiveness to histamine but that other as yet undefined factors must also contribute to the differences that exist among dogs in their pulmonary responsiveness to bronchoconstrictor agents.

Adrenergic beta-Antagonists↗
PubMed1981

Reanalysis of the refractory period in exertional asthma.

In an effort to determine whether the refractory period in exercise-induced asthma derived from mediator consumption we had seven asthmatic subjects repeatedly perform both exercise and eucapnic hyperventilation at matched minute ventilations under precisely controlled inspired air conditions. We reasoned that, if airway cooling were causing an agent to be released whose depletion resulted in less responsiveness, we should be able to observe this phenomenon irrespective of how cooling was produced. Repetitive exercise at short intervals produced a diminution in the obstructive response that disappeared when the interval between challenges was extended to 2 h. However, the degree of obstruction that occurred after voluntary hyperventilation remained constant irrespective of when the provocations were performed and equaled that seen with the first and last exercise challenge. Because the thermal burdens were identical for each challenge and all time periods, these results are incompatible with mediator depletion and suggest that it may be the secondary sympathoadrenal consequences of repeated exercise that cause the airways to temporarily lose their responsivity.

Asthma↗