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Biomedical subjects

R H Ingram

Publications and source records attributed to R H Ingram.

At least 37 records · Page 2Linked to original sources
PubMed1978

Distribution of bronchodilatation in normal subjects: beta agonist versus atropine.

Bronchodilatation was produced in normal subjects by the inhalation of a parasympatholytic agent (atropine) and the response was compared to that occurring after the inhalation of a beta-adrenergic agent (isoetharine). Doses were chosen that resulted in equivalent increases in specific airway conductance (78 +/- 9% for atropine; 88 +/- 21% for isoetharine). Anatomic dead space and volume at the onset of the terminal nitrogen rise (closing volume) were measured before and after each agent. Although there was no difference in the degree of overall bronchodilatation after the two drugs, anatomical dead space increased significantly more after atropine than isoetharine (+17% vs. +6%, P less than 0.01), and closing volume increased significantly after isoetharine (P less than 0.005) but did not change with atropine. We interpret these differences to indicate a greater effect of cholinergic antagonists on the more central airways and a greater effect of beta-adrenergic stimulants on peripheral airways.

Adult↗
PubMed1978

Vocal cord closure. A cause of upper airway obstruction during controlled ventilation.

Studies of vocal cord function were undertaken in a quadriplegic patient requiring ventilatory assistance, and in 2 normal subjects during controlled ventilation in a tank-type respirator. When the patient and the normal subjects relaxed and made no conscious effort to assist the respirator, the vocal cords were observed to close during inspiration and a large pressure gradient (12 to 19 cm H2O) developed across the cords. When the subjects made a slight inspiratory effort ("assist" mode), the cords opened widely during inspiration. There were large increases in flow and tidal volume in the "assist" mode compared with passive ventilation. Measurements of transdiaphragmatic pressure and esophageal pressure showed that these variables did not increase with the slight assist. Thus, increase in ventilation during the "assist" mode appeared to be due to alleviation of inspiratory obstruction at the level of the vocal cords. The same phenomenon was observed in the patient during phrenic nerve pacing. A pacemaker was designed to be triggered by the electromyographic impulse from an accessory muscle of respiration. In this manner, vocal cord opening could be coordinated with the mechanical assist given by the phrenic nerve pacer.

Adult↗
PubMed1978

Problems in the plethysmographic assessment of changes in total lung capacity in asthma.

We studied the effect of abdominal gas compression on plethysmographically determined total lung capacity (TLC) in asthmatic patients before, during, and after treatment of induced bronchospasm. TLC was derived from panting maneuvers near residual volume, at functional residual capacity, and near TLC. Significant differences among these "derived TLC" values increased significantly during bronchospasm. Whether or not TLC appeared to increase, and by how much, depended on the level of the vital capacity from which it was derived. Individual increases in TLC during bronchospasm could not be explained by increases in abdominal gas volume or in the extent to which it was compressed and decompressed during panting. We postulate that during the Boyle's Law panting maneuver, pleural, and therefore alveolar, pressure swings may be nonhomogeneous and greater over lung regions subtended by closed airways than over regions in communication with the mouth. This would result in an underestimation of alveolar pressure swings as measured at the mouth and an overestimation of thoracic gas volume, and would account in large part for the observed increase in discrepancies between the "derived TLC" values in asthma as well as the dependence of apparent TLC changes on the level of the VC at which the panting maneuver is performed.

Asthma↗
PubMed1978

Influence of heat and humidity on the airway obstruction induced by exercise in asthma.

We examined the degree of airway obstruction that developed in eight asthmatics who exercised while breathing air under four conditions: (a) ambient room temperature and water content; (b) body temperature and ambient water content; (c) ambient room temperature fully saturated; and (d) body temperature fully saturated. These test conditions were performed in random order. Multiple aspects of pulmonary mechanics were measured before and 5 min after exercise. When air at ambient conditions was inhaled, the expected airway obstruction developed after exercise, and all variables changes significantly from their pre-challenge values. Heating the air to body temperature did not influence this response. Increasing the humidity at ambient temperatures significantly blunted the response, and by inhaling body temperature, fully saturated air completely prevented it from occurring. Thus, the water content of inspired air is an important variable in the development of exercise induced asthma.

Adult↗
PubMed1977

Enhancement of exercise-induced asthma by cold air.

To study the possibility that the inhalation of cold air accentuates the bronchoconstrictor response to exercise in asthma, eight subjects exercised while breathing air at ambient or subfreezing temperatures. On a separate day, cold air was breathed at rest so as to isolate the effects of this stimulus. Pulmonary mechanics were measured before and after each experiment. In all subjects acute bronchoconstriction followed the control exercise challenge. With cold-air breathing, however, the magnitude of the response was markedly enhanced. Residual volume increased 158 per cent more than it did previously, and specific conductance and one-second forced expiratory volumes changed an additional 85 and 100 per cent, respectively. The effects of cold air at rest were very small. The results demonstrate a positive interaction of two common naturally occurring stimuli in the induction of asthmatic attacks, and constitute objective verification of a frequent clinical complaint.

Adult↗
PubMed1977

Cardiovascular effects of increasing airway pressure in the dog.

In paralyzed anesthetized dogs the cardiovascular effects of increasing positive end-expiratory pressure (PEEP) were explored under two conditions: a) end-expiratory lung volume increasing, b) end-expiratory lung volume kept nearly constant by matching pleural pressure rise to end-expiratory airway pressure rise. Two series of experiments were done: I) xenous return was allowed to fall, II) venous return was kept constant by infusion of volume. Right atrial pressure, pulmonary arterial pressure, and left atrial pressure increased under all conditions when measured relative to atmospheric pressure, but increased relative to pleural pressure only under condition a. The rise in left atrial relative to pleural pressure may indicate a degree of left ventricular dysfunction associated with increasing end-expiratory lung volume. Furthermore, when end-expiratory lung volume increased, inequality of the rise in pulmonary artery wedge pressure exceeded the rise in left atrial pressure in series I. From plots of cardiac output as a function of right atrial pressure it was possible to conclude that the decrease in venous return is partially offset by an increase in mean circulatory pressure.

Airway Resistance↗
PubMed1977

Effects of decreasing lung compliance with oleic acid on the cardiovascular response to PEEP.

In 12 anesthetized mongrel dogs on a constant volume ventilator, the response of the cardiovascular system to increasing positive end-expiratory pressure (PEEP) was examined before and after inducing acute lung injury with oleic acid. As PEEP was raised to approximately 16 mmHg, lung volume increased by approximately 900 ml before oleic acid and only 350 ml after. Pleural pressure increased by the same amount, indicating that both lung and chest wall compliance decreased with oleic acid. Right atrial pressure, the back pressure to venous return, also increased by the same amount. Although cardiac output at PEEP = 0 was lower after oleic acid, the relative decrements produced by increasing PEEP were the same as before oleic acid.

Animals↗
PubMed1977

Relative contributions of hypocarbia and hyperpnea as mechanisms in postexercise asthma.

The purpose of this investigation was to assess the relative contributions of hyperpnea and hypocapnia in the induction of postexercise asthma. To achieve these ends, eight young asthmatics were exercised on a treadmill while minute ventilations (VE) and end-tidal CO2 (PET CO2) tensions were continuously recorded. The subjects were then restudied using a partial rebreathing technique that allowed separation of minute and alveolar ventilations so that independent evaluations could be made of the relative effects of bulk airflow on pulmonary mechanics as well as a systematic study of hypocapnia in a dose-response fashion. Sustained hyperpnea with VEidentical to those recorded during exercise was totally without effect when the mean PET CO2 was isocapnic or lowered to approximately 30 Torr. Reduction in PETCO2 to 21.3 +/-0.9 Torr brought about significant changes in mechanics, but in every variable measured, exercise produced the greatest alterations and did so at PETCO2 values that had no effect when studied in a controlled fashion. Consequently, neither high VE per se, nor hypocapnia can be considered as the mechanisms underlying exercise induced asthma.

Adult↗
PubMed1977

Effects of intravenous histamine on pulmonary mechanics in nonasthmatic and asthmatic subjects.

Histamine is thought to be one of the primary mediators of the airways response in allergic asthma. We have studied in detail in nonasthmatic and asthmatic volunteers the effects of its intravenous infusion on pulmonary mechanics. The doses used were similar in both groups and limited by vascular rather than pulmonary effects. Measurements were made of lung resistance, the subdivisions of lung volume, maximal flow, density dependence, lung elastic recoil and dynamic compliance. The only mean group changes were a decrease in dynamic compliance and increase in frequency dependence of compliance in the nonasthmatics. Although in nonasthmatic individuals, statistically significant changes occasionally occurred in some parameters, the response was variable on repeated studies and sufficiently small to be of questionable physiological significance. Some of the asthmatics developed larger changes, but these only occurred in those individuals whose preinfusion pulmonary function was abnormal. Our results suggest the possibility that altered prechallenge pulmonary function rather than an unusual sensitivity to histamine may determine the greater responses observed in asthmatics.

Adult↗
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↗