Search PubMed⌕ Search

Biomedical subjects

R H Ingram

Publications and source records attributed to R H Ingram.

At least 145 records · Page 8Linked to original sources
PubMed1977

Airway responses to inhaled histamine in asymptomatic smokers and nonsmokers.

Bronchia reactivity to inhaled histamine was assessed in asymptomatic cigarette smokers and in nonsmoking atopic and nonatopic subjects. The only prechallenge between-group difference was the ratio of maximal flow on 80% helium-20% oxygen (Vmax HeO2) to maximal flow on air (Vmax air) from partial expiratory flow volume curves at 25% vital capacity (25% VC PEFV): Mean +/- SEM for smokers 1.18 /+- 0.06, atopics 1.45 +/- 0.08, nonatopics 1.51 +/- 0.03. This suggests that prior to inhalation to total lung capacity, the predominant site of resistance at flow limitation was in smaller airways of the smokers and in larger airways of both groups of nonsmokers. Following inhalation of histamine, smokers and nonatopics had similar changes in lung volumes and Vmax air which were less than in atopics. The Vmax HeO2/Vmax air ratios at 25% VC PEFV increased in smokers and decreased in nonsmokers: smokers 1.48 +/- 0.08, atopics 1.22 +/- 0.10, nontopics 1.16 +/- 0.06. This suggests a predominant large airway response in smokers and a prominent small airway response in nonsmokers. These responses may reflect differences in the predominant site of aerosol deposition rather than in airway reactivity.

Adult↗
PubMed1977

Comparison of arm versus leg work in induction of acute episodes of asthma.

The severity of exercise-induced asthma varies with the type of exercise performed. To determine whether such variation could be attributed to the use of different muscle groups, we exercised arms separately from legs using a bicycle ergometer. First, arms were exercised to exhaustion, then legs were exercised at the same load for the same duration. Arm work resulted in greater ventilation, heart rate, hydrogen ion concentration, and airway obstruction than did leg work. Later, legs were exercised to exhaustion using a load more than twice that of the arm work. Both the exhausting leg work and exhausting arm work resulted in significant bronchospasm and acidosis, whereas the nonexhausting leg work did not. These data suggest that, in arm and/or leg exercise, the relationship of work load to muscle mass is a determinant of airway obstruction.

Adult↗
PubMed1977

Predominant site of flow limitation and mechanisms of postexertional asthma.

To determine if a relationship existed between the site of airway obstruction and the mechanisms of exercise-induced asthma, we studied the predominant site of flow limitation, as determined by the mid-vital capacity ratios of maximal expiratory flow with air (Vmax air) and 80% helium-20% oxygen (Vmax He-O2), before and after physical exertion in 12 asthmatics. These observations were then related to the effects seen after vagal blockade and inhibition of mediator release. Five subjects increased Vmax He-O2/Vmax air ratios suggesting that the predominant site of flow limitation was in large airways. This group had their postexercise bronchospasm abolished by pretreatment with an anticholinergic agent. Seven subjects decreased their flow ratios indicating predominant small airway obstruction. Anticholinergic agents, although producing bronchodilation, did not alter their bronchospastic response to exercise. However, pretreatment with disodium cromoglycate did significantly diminish the response of this group. Thus the airway response to exercise in asthmatics is heterogeneous in terms of predominant site of flow limitation and this factor appears to relate to mechanisms.

Adult↗
PubMed1977

Canine pulmonary response to aerosol histamine: direct versus vagal effects.

Histamine, a potent bronchoconstrictor, has been shown to produce bronchoconstriction both directly and by a vagal reflex. To define the relative roles of direct and reflex effects, we studied the pulmonary response of dogs exposed to increasing doses of aerosol histamine before and after vagal blockade or vagotomy. In addition, the relative contributions of aerodynamically large and small airways to the overall response were determined by the measurement of pulmonary resistance on sulfur hexafluoride-oxygen and helium-oxygen mixtures. Histamine aerosol caused a similar dose-dependent increase in resistance of aerodynamically large and small airways and fall in dynamic compliance. The dose-response relationships were not consistently altered by either vagal blockade or vagotomy. The following variables were found not to alter the experimental results: anesthesia, type of aerosol generator, control of breathing during aerosol exposure, spontaneous breathing vs. controlled ventilation after aerosol exposure, cold block of vagi vs. vagotomy. We conclude that 1) histamine aerosol in dogs causes a local dose-dependent constriction of bronchial smooth muscle, and 2) the vagus nerve played a relatively minor role in the pulmonary response to aerosol histamine in these experiments.

Aerosols↗
PubMed1977

Arterial oxygenation differences with carbon dioxide-induced versus voluntary increases in minute ventilation in chronic airway obstruction.

Two groups of patients with similar degrees of chronic airway obstruction exhibited different degrees of increased arterial oxygenation with CO2-induced hyperpnea versus voluntary increases in ventilation matched for ventilatory pattern. Patients who failed to increase arterial PO2 as much with voluntary hyperventilation as with CO2 challenge also had a lower dynamic compliance with the voluntary maneuver, whereas those with similar increases in arterial PO2 had similar dynamic compliances during the 2 periods of increased minute ventilation. The differences between the 2 groups are believed to be related to different effects of hypocapnia on collateral ventilation.

Airway Obstruction↗
PubMed1977

Influence of abdominal pressure and sympathetic vasoconstriction on the cardiovascular response to positive end-expiratory pressure.

The role of changes in abdominal pressure and sympathetically mediated vasoconstriction in the cardiovascular response to positive end-expiratory pressure was evaluated in 9 mongrel dogs. When the abdomen was widely opened, the decrease in cardiac output caused by positive end-expiratory pressure was the same as that found during control studies. When the abdomen was tightly bound, cardiac output was higher at any positive end-expiratory pressure than in control state (P less than 0.01), but the percent decrease produced by increasing positive end-expiratory pressure was the same. alpha-Adrenergic blockade with phenoxybenzamine produced a significantly greater decrease in cardiac output at any given positive end-expiratory pressure and thus appeared to inhibit the previously operative peripheral vascular adjustments to positive end-expiratory pressure. The major compensatory mechanism in the cardiovascular response to positive end-expiratory pressure thus appears to be mediated via alpha-adrenergic sympathetic factors.

Abdomen↗
PubMed1977

Relative contributions of large and small airways to flow limitation in normal subjects before and after atropine and isoproterenol.

Bronchodilatation was produced in normal subjects by the inhalation of atropine, a parasympatholytic agent, and isoproterenol, a beta adrenergic stimulator. Density dependence of maximal expiratory flow (Vmax), expressed as a ratio of Vmax with an 80% helium-20% oxygen gas mixture to Vmax with air at isolung volumes, indicated that the predominant flow regimes across upstream airways changed differently after each agent was given separately. After atropine Vmax increased, elastic recoil pressure did not change, and density dependence decreased. Utilizing the equal pressure points analysis which defines upstream and downstream segments of the intrathoracic airways at flow limitation, these results suggest a greater relative dilatation of the larger upstream airways such that more of the driving pressure is dissipated across the smaller airways in which flow is less dependent upon gas density. After isoproterenol Vmax increased, elastic recoil pressure did not change, and density dependence increased. This suggests a preferential dilatation of the smaller and more peripheral airways with less density-dependent flow regimes such that more of the driving pressure would be dissipated in the larger airways in which flow is more dependent upon gas density. Systematic decreases after isoproterenol lead independently to the same conclusion. After both agents together, Vmax increased and density dependence and critical alveolar pressures did not change from control, suggesting a relatively uniform dilatation of all the airways comprising the upstream segment.

Adult↗
PubMed1977

A critical assessment of the roles of circulating hydrogen ion and lactate in the production of exercise-induced asthma.

To evaluate the roles of circulating hydrogen ion and lactate in the production of exercise-induced asthma, two experiments were performed. In the first, we exercised six asthmatic subjects to exhaustion on a bicycle ergometer while recording arterial pH at periodic intervals. Multiple aspects of pulmonary mechanics were measured before and after the work load. After recovery, the identical procedures were repeated, but sufficient quantities of sodium bicarbonate were infused to keep the pH at the pre-exercise level. In both experiments, statistically identical attacks of asthma were induced. To study the effect of lactate, five subjects were exercised on several occasions in order to determine the lowest level of work, and hence arterial lactate, that was reproducibly associated with an acute asthma attack. When this was known, sufficient quantities of sodium lactate were infused into the resting subjects so as to equal or exceed the amount produced with exercise. Pulmonary mechanics were not altered with this intervention. These findings demonstrate that lactic acidemia is not the cause of exercise-induced asthma.

Acidosis↗
PubMed1976

Density-dependence of maximal expiratory flow rates before and after bronchodilators in patients with obstructive airways disease.

1.Gas-density-dependence of maximal expiratory flow rats (V max), defined as the ratio of V max. while breathing helium/oxygen (80:20) to V max. while breathing air at the same lung volume, was examined in relation to other measurements of airways obstruction in patients with obstructive airways disease before and after administration of bronchodilators. 2. Seventeen patients showed a 45% or greater increase in specific conductance (sG aw) after bronchodilator therapy (group A) and thirteen patients demonstrated a lesser response (group B). 3. Before the administration of bronchodilators, the degree of obstruction in two groups was not different as measured by lung volumes, sG aw, forced expiratory volume in 1 s, and flow rates high in the vital capacity; yet the maximal mid-expiratory flow rate and the degree of density-dependence were significantly lower in group B. 4. After bronchodilators, both groups of patients showed significant improvements in sG aw, flow rates and lung volumes. However, group A patients showed a signifcant increase in density-dependence whereas group B patients did not. 5. Increased density-dependence after bronchodilators in the group A patients was associated with an increase in the computed resistance of the upstream segment with air and a decrease in resistance with helium/oxygen. These changes could be explained by a more mouthward of equal pressure points, and therefore a further increase in the relative contribution of the larger density-dependent airways to limitation of flow. 6. The fact that density-dependence was not altered after bronchodilators in the group B patients suggests that the site of limitation of flow did not change appreciably. The shift in the pressure-flow curve for the upstream airways was such that the computed resistance of these airways fell. Thus it appears that the airways comprising the upstream segment were dilated.

Airway Obstruction↗
PubMed1976

Relationship of AaDO2 TO AIRWAY PCO2 in dog lungs.

We measured the arterial Po2 and AaDo2 in open-chest dogs respired with air and with 5% CO2 in air at various lung volumes using a constant hyperventilatory pattern. The AaDo2 was an inverse function of lung volume with both air and 5% CO2 and was also an inverse function of both alveolar and arterial Pco2 values except at quite high lung volumes. There were two series of closed-chest experiments. In the first series, ventilation was varied to produce alveolar Pco2 and Po2 changes. In the second series, the dogs were hyperventilated at a constant rate and Pco2 was varied by adding CO2 with alveolar Po2 levels kept relatively constant. In both series the AaDo2 was inversely related to Pco2. We conclude that, in dogs, the AaDo2 is independent upon the Pco2 and speculate that this may be related to the effect of CO2 on collateral ventilation, although the Bohr effect may account for some of the dependence.

Airway Resistance↗
PubMed1976

Effect of volume history on successive partial expiratory flow-volume maneuvers.

In normal subjects, the second of two successive partial expiratory flow-volume (PEFV 2) curves often had higher isovolume maximal expiratory flow rates (Vmax) than the first (PEFV 1) (mean increase 30.2 +/- 13%). The higher Vmax on PEFV 2 was present only when there was a greater lung elastic recoil pressure (Pst(L)). In eight subjects the Pst(L) derived from sequential partial quasi-static pressure-volume curves, from interruption of the flow-volume maneuvers and at the start of the PEFV curves showed that isovolume upstream resistance increased although Vmax also increased after going to residual volume (RV). In four subjects the RV volume history did not change the pressure flow relationship across the upstream airways. If airways dimensions were the sole determinant of Vmax, then Vmax on PEFV 2 would be the same or smaller than on PEFV 1. That the opposite was observed in our study indicates that the increase in Pst(L), which results from parenchymal hysteresis, offsets any dimensional decrease in upstream airways due to airways hysteresis.

Adult↗
PubMed1976

Distribution of pulmonary resistance: effects of gas density, viscosity, and flow rate.

Theoretical predictions of the distribution of inspiratory viscous pressure loss were made for canine and human pulmonary airways for gases with varying density and viscosity at different pulmonary flow rates. We predicted that in canine or human airways when tracheal flow was turbulent, most of the total calculated pressure loss would be in the first few branchings of the bronchial tree; however when tracheal flow was nearly laminar inspiratory pressure loss would be spread more uniformly along the airways. To test these predictions an airway catheter was used to partition total pulmonary resistance (RL) in five anesthetized dogs. On air the catheter was positioned such that the mean resistance mouthward of the catheter tip (Rc) at a flow of 0.5 1/s was 63% of RL. At the same catheter position Rc was 87% of RL when the dogs were breathing a mixture of 80% sulfur hexafluoride-20% oxygen and resistance was determined at 1.0 1/s. Rc was 50% of RL when the dogs were breathing a mixture of 80% helium-20% oxygen and resistance was determined at 0.25 1/s. Thus altering gas physical properties and flow rates changed the distribution of pulmonary resistance as predicted.

Airway Resistance↗
PubMed1976

Localization of airway constriction using gases of varying density and viscosity.

The relationship between the major site of airway constriction and change in total pulmonary resistance while breathing gases of varying density and viscosity was studied in five anesthetized dogs pretreated with atropine. Using an airway catheter, central and peripheral components of pulmonary resistance were measured by forced oscillation. Total pulmonary resistance was measured at 0.5 1/s with lungs air-filled, at 0.25 1/s with the lungs filled with 80% helium-20% oxygen (RL-He), and at 1.0 1/s with 80% sulfur hexafluoride-20% oxygen (RL-SF6). Intravenous histamine infusion resulted in a predominantly peripheral resistance increase as determined by the airway catheter and a much larger percentage increase in RL-He than in RL-SF6. Tracheal banding produced a purely central resistance increase and a greater change in RL-SF6 than in FL-He. These results support theoretical predictions that the predominant site of airways constriction can be determined without on airway catheter by comparing relative changes in total pulmonary resistance using different flow regimes.

Airway Resistance↗
PubMed1976

An assessment of the pulmonary response to exercise in asthma and an analysis of the factors influencing it.

The purposes of this study were to determine (1) whether an exercise stimulus could be repeatedly applied to a group of asthmatics and normal control subjects with reproducible metabolic and ventilatory consequences; (2) the effect of this stimulus on multiple aspects of pulmonary mechanics in both groups; (3) the degree of within- and between-day variation in response and the factors influencing it; and (4) the effects of pretreatment with disodium cromoglycate. Airway resistance, specific conductance, total lung capacity and its subdivisions, and forced expiratory volumes and flow rates were measured in 21 asthmatics and 8 normal control subjects before and after treadmill exercise. Minutes ventilation, tidal volume, repiratory frequency, oxygen consumption, carbon dioxide production, heart rate, and end-tidal carbon dioxide tensions were measured during exercise and recovery. The asthmatics were studied twice datly on 2 separate days. Disodium cromoglycate was administered to the asthmatics before the fourth trial. The control subjects were studied twice on the same day without any interventions. There was no difference between exercise trials as measured by any of the gas exchange variables and there were no within-day differences in baseline pulmonary mechanics in either group. In contrast to the control group, all of the asthmatics had increasing airway obstruction after the exercise challenge. There were no between -day differences in the baseline data or response to exercise in the asthmatics except that the mechanical response was less after disodium cromoglycate, which suggests that mediator release played a part. Although as a group the stimulus and response were reproducible, when data of each trial were related to the type and degree of baseline dysfunction there was a direct relationship between pre-existing obstruction and magnitude of response. This suggests that exercise-induced asthma is not an all-or-none event, but rather a continuum of responses profoundly influenced by the pre-challenge state of the airways.

Adolescent↗
PubMed1975

Effects of airway versus arterial CO2 changes on lung mechanics in dogs.

The effects of changes in airway CO2 partial pressure (PAco2) and arterial CO2 partial pressure (Paco2) on lung mechanics were studied in dogs by utilizing unilateral pulmonary artery occlusion and a tracheal divider which allowed separate variation of PAco2 and Paco2. When Paco2 was held at a reasonably normal level, lower than normal PAco2 levels resulted in large compliance decreases, alteration of the complete static pressure-volume curves, and increases in resistance. Invreases in PAco2 to hypercapnic levels did not produce changes. When PAco2 was held at a reasonably normal level, changes in Paco2 levels were positively and directly related to resistance with small and inconsistent effects on compliance and on complete static pressure-volume curves. A combination of low PAco2 and high Paco2 produced large increases in resistance, alterations of the static pressure-volume curve, and decreases in compliance. Vagotomy during the combined stimulus resulted in only a decrease in resistance without change in lung elastic properties. The results suggest that the mechanical effects of airway hypocapnia and systemic hypercapnia are additive. However, small airways effects of low PAco2 appear to be maximal and uninfluenced by the vagally mediated response to Paco2 increases.

Animals↗
PubMed1975

Relationship of phase IV to closing volume in lateral body positions.

We studied the effect of body position in humans on the relationship between exhaled vital capacity (VC) and both helium (He) and nitrogen (N2) concentrations after delivery of an He bolus at residual volume (RV) followed by 100% oxygen to total lung capacity. Phase IV, defined as the % VC at the first sharp and permanent increase in N2 and He, occurred at a mean of 15.7% VC while seated, 60.0% VC in right lateral and 59.6% VC in left lateral positions. He bolus delivery above RV but well below 60% VC resulted in the disappearance of phase IV. Lung pressure-volume (PV) curves had inflections at the volume of phase IV in the seated position: but the inflections were well below phase IV in lateral positions. Phase IV increased to higher volumes at higher mouth pressures. The relationship between phase IV and mouth pressure fell near the respiratory system relaxation PV curves. The findings suggest the higher phase IV in lateral positions is due to sequence of emptying without airway closure and is influenced by active expiration.

Helium↗