No description available.

This research was undertaken in order to investigate the robustness of the Anzai respiratory gating system. Tests were performed to verify the transfer of image data, to identify the method of gating and the accuracy of phase identification. It was found to have sizeable limitations which could result in either incorrectly gated images or serious artefacts. For these reasons it is recommended it be used under the guidance of a suitably qualified physicist.

No description available.

The pressure-flow characteristics of inspiration have been studied, with particular reference to breathing dense gas at raised environmental pressure. The inspiratory pressure-flow relationship was determined from maximal and submaximal breaths performed by divers at pressures equivalent to 18, 39 and 56 msw, and compared with the relationship measured at sea level. Inspiratory flow limitation was found at every depth, becoming more severe as environmental pressure was increased. Similar studies performed at sea level in subjects breathing dense gas mixtures or breathing against a fixed resistance also showed some evidence for inspiratory flow limitation. Evidence was also found for sudden, transient flow interruptions breathing dense gas at raised environmental pressure and at sea level. An additional effect of high pressure on inspiration was observed, which leads to a distinctive pattern of oscillatory flow and which may be related to the High Pressure Neurological Syndrome. Flow oscillations developed in divers suffering from HPNS. These were of the same frequency range as muscle tremors associated with the syndrome. A mechanism of dynamic inspiratory airway compression has been proposed to explain these results.

Experiments were performed to elucidate the mechanisms contributing to the hyperbaric bradycardia. Ethical approval was obtained and all subjects gave written and informed consent. Heart rate, arterial blood pressure, respiratory activity and carotid sinus baroreceptor reflexes were monitored non-invasively. Four healthy male saturation divers were compressed to 46ATA. Significant reductions in resting heart rate, mean arterial pressure, systolic blood pressure and diastolic blood pressure were observed. Baroreceptor sensitivity was significantly increased at 46ATA. A separate series of investigations determined the effects of breathing an increased gas density and an increased partial pressure of oxygen (<I>P</I>₀₂) on arterial blood pressure, heart rate and baroreceptor sensitivity at 1ATA. Two groups of 6 healthy male subjects participated in the experiments. No significant changes in resting heart rate, arterial blood pressure, respiratory rate, tidal volume or baroreceptor sensitivity were observed breathing an increased gas density up to 5.47gl^-1. Raising the inspired <I>P</I>₀₂ to 0.5bar at 1ATA resulted in a significant reduction in resting heart rate and a significant increase in carotid sinus baroreceptor sensitivity. Respiratory sinus arrhythmia (RSA) was used as a non-invasive estimate of vagal tone to determine whether the hyperbaric bradycardia is associated with changes in vagal autonomic control. No changes in the overall magnitude of RSA were observed over a range of respiratory rates at high pressure compared to controls at 1ATA. These results suggest that increased gas density is not a contributing factor but increased <I>P</I>₀₂ may play a role in the development of hyperbaric bradycardia.

Bronchial hyperreactivity to non-allergic stimuli in allergic subjects can be measured by the increased bronchomotor response to the inhalation of controlled low concentrations of sulphur dioxide (5-20 ppm). This bronchomotor response is graded from the normal subjects and patients with chronic bronchitis who had the smallest response, to the atopic subjects with an intermediate response, to the asthmatic patient with the largest response. Allergic subjects could be distinguished from the non-allergic subjects by the intensity of this response, but it was not possible to consistently discriminate between asthmatic and non-asthmatic allergic subjects. Measurements of maximal flow at low lung volumes suggest that the site of action is in the intrathoracic as well as extrathoracic airways. The bronchomotor response to exercise, another non-allergic stimulus depends on the degree of airway cooling as determined by the temperature and humidity of the inspired air. The mechanism of action of irritant gas stimulation is multifactorial. The cholinergic reflex pathway has an important role as shown by the results of respiratory reflexes and efferent cholinergic blockade. However, this pathway seems to be relatively more important in allergic but non-asthmatic subjects than in patients with lower airway problems. Also, this mechanism is variable in patients with asthma. Another mechanism is that of mast cell release of mediators of anaphylaxis. Studies with a stabilizer of the mast cell membrane disodium cromoglycate, and an H₁ receptor antagonist clemastine, provide convincing indirect evidence of the importance of this mechanism in non-allergen triggered bronchoconstriction. However, in exercise-induced bronchoconstriction, a rise in plasma histamine is random and is probably the result of the stress of exercise and not the cause of bronchoconstriction. A definitive answer necessitates measurements of histamine in pulmonary venous blood, studies of the modulating effect of inhaled specific antagonists to histamine and other mediators on exercise-induced asthma.

No description available.

The effect of heavy load carriage on pulmonary function at rest and on breathing pattern and lung volumes during graded exercise was studied. Fifteen males completed treadmill tests to measure VO2peak with and without a 25-kg pack. Subsequently, each subject completed short periods of treadmill walking in loaded and unloaded conditions at intensities equivalent to 55, 65, 75 and 85% of VO2peak. At rest, in the loaded condition, forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) both were reduced by 3% with no change in FEV1/FVC. During exercise with the pack, tidal volume (VT) and end-inspiratory lung volume (EILV) were reduced by 14 and 5%, respectively, while ventilation (VE) was maintained by a 9% increase in breathing frequency (Bf). Rating of perceived exertion (RPE) was always higher during the loaded trial, despite identical oxygen consumption (VO2) and heart rate (HR) responses. During graded exercise under heavy load up to 85% of VO2peak, breathing pattern is altered to maintain VE while respiratory mechanics were not altered.

Bibliography: leaves 217-244. / x, 246 leaves : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Tachykinins are implicated in the mediation of airway inflammatory responses and may have roles in airway remodeling and healing. The actions of tachykinins are mediated by specific receptors, designated NK1, NK2 and NK3. Tachykinin degredation, an important mechanism for limiting the effects of these peptides, is principally mediated by neutral endopeptidase (NEP). This thesis investigates the role of tachykinins, in vivo, in an ovine model and in human airway epithelium. Results show that the nett effect of tachykinins in the airway will depend on the relative balance between the expression of receptors, tachykinins and NEP. Assessment of these molecules in the airway epithelium from subjects with normal lungs or chronic bronchitis showed that preprotachykinin-A gene expression was relatively higher in the disease group whereas NEP and NK1 receptor levels were unchanged. These studies provide new insights into the role of tachykinins in airways disease. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999

Thesis (M.P.H.)--University of Adelaide, Dept. of Community Medicine, 1988. / Includes bibliographical references (leaves 161-192).