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Biomedical subjects

R H Ingram

Publications and source records attributed to R H Ingram.

At least 127 records · Page 7Linked to original sources
PubMed1978

Influence of abdominal gas on the Boyle's law determination of thoracic gas volume.

In a body plethysmograph we have demonstrated differences in total lung capacity (TLC) derived from panting maneuvers performed at different levels in the vital capacity. In almost all cases, the discrepancies were due to the magnitude of the abdominal gas volume (AGV) and the relative magnitude of abdominal and thoracic pressure swings during the panting mandeuver. When panting was performed at functional residual capacity (FRC), the effect of AGV compression on the determination of thoracid gas volume (TGV) was small. Of 11 individuals studied 2 were known to have mild asthma. Compression and decompression of AGV appeared to be an insufficient explanation for discrepancies in derived TLC's in these two, suggesting that other as yet unidentified factors may influence the plethysmographic determination of TGV.

Gases↗
PubMed1978

Distribution of pulmonary responsiveness to aerosol histamine in dogs.

Dose-response curves to aerosol histamine in 102 anesthetized, intubated, spontaneously breathing dogs revealed a spectrum of airway responsiveness with a greater than 40-fold difference between the most and the least sensitive animals. The frequency distribution of responses fits a log normal distribution. No correlation was found between sex, age, or control values of dynamic compliance (Cdyn) and lung resistance (RL) and the dose of histamine required to cause a response. Repetitive studies in 17 dogs observed for up to 20 mo showed that the dose at which an individual dog would respond was reproducible within a narrow range and that the differences between dogs were highly significant (P greater than 0.001). The long-term reproducibility of the response to aerosol histamine in individual dogs suggests that short-term reversible airway insults are not responsible for the range in responses noted between animals.

Aerosols↗
PubMed1978

Vagal and aerosol histamine interactions on airway responses in dogs.

Histamine aerosol was administered to 10 anesthetized paralyzed artificially ventilated dogs whose vagi were first intact, then cut, and then peripherally stimulated. Pulmonary resistance (RL) was measured and dose-response curves determined in the three conditions. The dogs were divided into two groups based on the initial response to histamine with the vagi intact. The low-dose (LD) group had a greater than or equal to 50% increase in RL when exposed to a histamine concentration of 1.0 mg/ml. The high-dose (HD) group had a greater than or equal to 50% increase in RL when exposed to an aerosol containing 3.0 mg/ml histamine or more. In both groups there was a dose-related increase in RL with histamine with the vagi intact, cut, or stimulated. In three of the LD dogs there was a greater than additive interaction between vagal stimulation and inhaled histamine, whereas in the HD dogs the interaction was at most additive. With the vagi cut, both groups had a significantly lesser histamine response. The results show that differences in histamine responsiveness between dogs is in part related to varying degrees of nonreflex histamine-vagal interaction.

Aerosols↗
PubMed1978

Effects of atropine on potentiation of exercise-induced bronchospasm by cold air.

The role of vagal efferent activity in the cold air potentiation of exercise-induced asthma was assessed by exercising nine subjects who breathed air at ambient and subfreezing temperatures before and after cholinergic blockade. Lung volumes and maximal expiratory flow volume curves with air and with 80% helium-20% oxygen were obtained before and 5--10 min after each challenge. Isovolume comparisons of maximal expiratory flow rates with the two gases were used to assess relative contributions of large and small airways to flow limitation. Exercise under ambient conditions resulted in the expected airway obstruction and cold air exaggerated the response. Atropine pretreatment had no effect on the cold air potentiation. After atropine with ambient air exercise, there was an increase in the relative contribution of large airways to flow limitation, whereas exercise with cold air resulted in an increase in the contribution of small airways. We concluded that the potentiating effects of cold air are local and suggest that the immediate stimulus is related to cooling of intrathoracic airways.

Adult↗
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↗