Dissertations / Theses on the topic 'Anoxemia – Physiological effect'

The studies in this thesis assess the ventilatory and vascular effects of short-term awake isocapnic hypoxia in healthy subjects and those with obstructive sleep apnoea (OSA). The particular focus of this thesis is the impact of the hypoxic stimulus on indices of arterial stiffness, in particular the augmentation index (AIx) and time to reflection (Tr). The role of nitric oxide in this response in healthy subjects is also examined.

Clinical studies have demonstrated an arousal deficit in infants suffering Obstructive Sleep Apnoea (OSA), and that treatment to alleviate the symptoms of OSA appears to reverse the deficit in arousability. Some sudden infant deaths are thought to be contingent upon such an arousal deficit. This research utilised young piglets during early postnatal development, and exposed them to intermittent hypercapnic hypoxia (IHH) as a model of clinical respiratory diseases. Arousal responses of control animals were compared to the animals exposed to IHH. Comparisons were also made between successive exposures on the first and the fourth consecutive days of IHH. Time to arouse after the onset of the respiratory stimulus, and frequency of arousals during recovery, demonstrated that arousal deficits arose after successive exposures and that these were further exacerbated on the fourth study day. After an overnight recovery period, the arousal deficit was apparently dormant, and only triggered by HH exposure. These studies confirm that both acute and chronic deficits can be induced on a background of otherwise normal postnatal development, suggesting that deficits observed in the clinical setting may be a secondary phenomenon.

Master of Science (Medicine)
Clinical studies have demonstrated an arousal deficit in infants suffering Obstructive Sleep Apnoea (OSA), and that treatment to alleviate the symptoms of OSA appears to reverse the deficit in arousability. Some sudden infant deaths are thought to be contingent upon such an arousal deficit. This research utilised young piglets during early postnatal development, and exposed them to intermittent hypercapnic hypoxia (IHH) as a model of clinical respiratory diseases. Arousal responses of control animals were compared to the animals exposed to IHH. Comparisons were also made between successive exposures on the first and the fourth consecutive days of IHH. Time to arouse after the onset of the respiratory stimulus, and frequency of arousals during recovery, demonstrated that arousal deficits arose after successive exposures and that these were further exacerbated on the fourth study day. After an overnight recovery period, the arousal deficit was apparently dormant, and only triggered by HH exposure. These studies confirm that both acute and chronic deficits can be induced on a background of otherwise normal postnatal development, suggesting that deficits observed in the clinical setting may be a secondary phenomenon.

Exercise-induced hypoxemia is a common observation in endurance-trained athletes. The present study examined the kinetics of oxyhemoglobin saturation during upright (UP) maximal cycling exercise in 84 healthy, untrained subjects between 8 and 26 years old. The prevalence of oxyhemoglobin desaturation (DS: SaO$ sb2 $ 0.05). A subgroup of children (n = 6) repeated the maximal exercise protocol in the supine (SU) position. In NDS values of SaO$ sb2$ were not affected by posture (UP: 95.3 $ pm$ 2.3 vs SU: 94.1 $ pm$ 0.9) for similar VO$ sb{ rm 2max}$ (UP: 3.7 $ pm$ 0.36 vs SU: 3.43 $ pm$ 0.36) (p $>$ 0.05). These observations suggest that exercise-induced DS is independent of age or training status. Differences due to posture may be related to variations in ventilatory and/or pulmonary perfusion parameters.

Embryos of the annual killifish Austrofundulus limnaeus display a remarkable tolerance to anoxia during development, most notably during embryonic diapause. Little is known about the metabolic or enzymatic changes that accompany this state of anoxia tolerance. This study examined the metabolic changes associated with exposure to anoxia by measuring the activity of the enzyme phosphoenolpyruvate carboxykinase (PEPCK), and by profiling the concentration of 31 metabolites ranging from amino acids to citric cycle intermediates at 4 different developmental stages, diapause 2 (DII), 4 days post diapause (dpd), 12 and 22 dpd. Embryos of A. limnaeus showed stage specific changes in concentrations of several metabolites. The most notable changes in metabolite concentration in response to anoxia were the increases of lactate, alanine, GABA and succinate as well as a pronounced decrease in aspartate concentrations. However, a complete understanding of the mechanisms by which anoxia tolerance is achieved remains elusive. Further studies into the tissue specific responses of anoxia would enable greater resolution when attempting to explain changes in concentrations of metabolites both during development and in response to anoxic insult.

Thesis (MPhil (Physiological Sciences))--University of Stellenbosch, 2006.
The responses of central systems to oxygen deprivation have been well characterised while adaptations in peripheral systems, such as skeletal muscles, have presented confounding variations. Several reasons for these discrepancies are purported, amongst them being the duration of exposure to hypoxia and variations in fibre composition. Moreover, in real-life high altitude situations there may be a combination of factors which have the ability to modify or alter the effect of hypoxia. This study investigates the effect of short duration hypoxia per se on substrate utilisation in different types of skeletal muscles.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.
ix, 108 leaves : ill. ; 29 cm

Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine and Royal Adelaide Hospital, Rheumatology Unit, 2004.
Includes list of publications arising from this thesis. Erratum attached to inside back cover. "25/03/2004." Includes bibliographical references (leaves 185-257).

On sait depuis longtemps que l’exposition à l’altitude est associée à une réduction de l’aptitude aérobie. Différentes hypothèses ont été posées pour expliquer cette limitation à l’effort en hypoxie (une limitation ventilatoire ou diaphragmatique, une altération de la diffusion pulmonaire et une disconcordance entre de la perfusion et la diffusion tissulaire, etc.) mais généralement, la limitation de l’effort aérobie en hypoxie est attribuée à une diminution du transport sanguin de l’O2 (TO2) parc convection vers les muscles. Le TO2 dépend du débit cardiaque (Q) et du contenu artériel en O2 (CaO2).

Le CaO2 est diminué en altitude à cause d’une diminution de la pression partielle inspirée en O2. Cependant, le chémoréflexe hypoxique tente de contrebalancer cet effet en élevant la ventilation et en diminuant la pression alvéolaire en CO2 afin de maintenir la pression alvéolaire en O2 constante. De plus, avec l’acclimatation, le rein produit de l’érythropoïétine permettant au taux d’hémoglobine d’augmenter. Ces deux principales adaptations à l’altitude ramènent le CaO2 à sa valeur de base du niveau de la mer en 2 à 3 semaines passées à 5000 m d’altitude mais sans amélioration de l’aptitude à l’effort aérobie.

L’exposition à l’altitude est aussi associée à une diminution du Q maximal. Les mécanismes à l’origine de cette limitation du Q maximal restent, à l’heure actuelle, incompris. Les principales explications évoquées sont, une diminution de la réserve chronotrope, une diminution de la commande nerveuse centrale vers le cœur ou une diminution de la demande périphérique. Récemment, des études sur des sujets sains en hypoxie suggérèrent qu’au moins une partie de la limitation du Q maximal à l’effort est liée à une élévation de la postcharge ventriculaire droite suite à l’hypertension pulmonaire induite par l’hypoxie. C’est cette hypothèse que nous avons voulu vérifier dans une première étude.

Nous avons étudié l’effet d’une inhibition de l’hypertension pulmonaire d’altitude par le sildénafil, un inhibiteur de la phosphodiestrérase-5, chez des sujets sains, en normoxie, en hypoxie aiguë et en hypoxie chronique. Les résultats de cette étude ont confirmé l’effet vasodilatateur pulmonaire du sildénafil et une augmentation de la VO2max en hypoxie aiguë. Cependant, la prise de ce dernier était couplée à une amélioration de l’oxygénation, si bien que l’élévation de la performance aérobie observée en hypoxie aiguë sous sildénafil ne pouvait être entièrement attribuée à une réduction de l’hypertension pulmonaire.

Nous conclurent que cette amélioration de la performance était probablement d’avantage liée à une amélioration de l'oxygénation qu’à un effet vasodilatateur pulmonaire.

Les résultats équivoques obtenus lors de cette première étude nous ont incité à tester les effets d’une amélioration de l’oxygénation sur la performance aérobie en haute altitude. Pour ce faire, quinze sujets sains ont été testés au niveau de la mer et après acclimatation à 4700 m d’altitude soit sous placebo, soit sous acétazolamide, un inhibiteur de l’anhydrase carbonique augmentant l’oxygénation par stimulation ventilatoire en réponse à une acidose métabolique. La prise d’acétazolamide n’eut aucun effet sur l’hémodynamique pulmonaire et sur la VO2max et la charge maximale. Nous avons toutefois observé qu’une amélioration de l’oxygénation durant l’effort retarde l’apparition du seuil ventilatoire améliorant ainsi la phase aérobie de l’effort. Cette étude confirme donc qu’une élévation du CaO2 permet une amélioration de l’aptitude aérobie.

Finalement, la dernière étude a pour but d’étudier les effets isolés d’une vasodilatation pulmonaire sur la performance aérobie en altitude. Les résultats d’une étude préliminaire montrent que l’inhibition de la vasoconstriction hypoxique par un agent pharmacologique antagoniste des récepteurs de l’endothéline ETA et ETB, le bosentan, permet une élévation de l’aptitude aérobie en hypoxie aiguë, sans effets sur l’oxygénation, confirmant ainsi notre hypothèse initiale qu’une postcharge ventriculaire droite augmentée en hypoxie peut contribuer à une limitation de l’aptitude à l’effort aérobie en hypoxie.

Conclusions :

L’ensemble de nos résultats suggère que l’aptitude aérobie en altitude est déterminée par le transport d’O2 qui peut être augmenté par manipulation pharmaceutique du débit ventriculaire droit maximal après inhibition de la vasoconstriction pulmonaire hypoxique (bosentan), amélioration de l’oxémie (acétazolamide) ou des deux (sildénafil).

Agrégation de l'enseignement supérieur en kinésithérapie et réadaptation
info:eu-repo/semantics/nonPublished

Bibliography: leaves 246-280.
xxi, 280 leaves : ill. (some col.) ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Identifies that exercise-induced hypoxemia occurs at a much lower exercise intensity than reported previously and that exercise mode changes the severity of the phenomonen.
Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999

The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been considered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more recent literature. Previously this phenomenon has been described as a decrement in both arterial oxygen partial pressure (PaO₂) and oxy-haemoglobin saturation (SaO₂or SpO₂) with, particularly important for PaO₂, a lack of or inappropriate correction made for the change in body temperature during intense exercise. The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with an offset of approximately 1.3ºC, and were considered much more appropriate and relevant indicators of thermal changes during exercise. As an extension of the initial work active muscle temperature (vastus lateralis) was measured during the exercise test, demonstrating a significantly lower resting temperature than the oft-reported “core” temperatures (rectal and oesophageal) as well as a significantly greater increase in temperature in comparison to all other measurement sites. Overall, the results of this first study indicated that the physiologically relevant temperatures measured at the oesophageal and muscle sites differed markedly to the outdated rectal temperature measurement site and should be used as measures of thermal response when evaluating oxygen loading (oesophageal) or unloading (active muscle). Utilising the definition of EIH as a decrease in PaO₂ of ≥ 10 mmHg, the effect of temperature correcting PaO₂ was evaluated in the second study. Arterial blood gases measured simultaneously to the temperature measurements during the incremental exercise test were adjusted for the temperature changes at each site (every 1ºC increase in temperature will increase a PaO₂ value by ~5 mmHg). Whilst uncorrected PaO₂ values indicated an almost 100% prevalence of EIH in this group, oesophageal temperature corrected PaO₂ values decreased this prevalence to ~50% while muscle temperature corrections resolved all cases of EIH and demonstrated an HYPEROXAEMIA (i.e. the reverse of the well-established phenomenon) in the majority of subjects. Further investigation of arterial oxygen content during the exercise test indicates that there is no disruption in the delivery of oxygen to the active muscles and therefore any performance decrement should be attributed to another mechanism. Whilst the phenomenon of EIH is determined by the definition applied and the use of temperature corrections in the case of PaO₂, its reproducibility in a test-retest situation had not previously been determined. Utilising a subset of previously tested subjects, the reproducibility of both temperature and PaO₂ were determined with results indicating that the blood gas response was highly reproducible, especially the minimum PaO₂ value noted during each exercise test. However, comparing a more statistically relevant definition of a change in PaO₂ of ± 2 standard deviations from the mean resting PaO₂ to the previous delimiter of 10 mmHg indicated a lesser reproducibility of the prevalence of EIH. In summary, this thesis exposes the inadequacies of previous research into EIH with regard to the expected reproducibility of the phenomenon and the need to correctly adjust PaO₂ values for exercise-induce hyperthermia as well as demonstrating the difference in thermal responses to acute exercise in physiologically significant areas of the body. Furthermore, previously described correlations between the change in PaO₂ and VO₂ max were not evident in the subjects tested within this thesis, nor was there any indication of a diffusion limitation based on reduced pulmonary capillary transit time (by association with VO₂ max) or pulmonary oedema (rebuked by a rapid return of PaO₂ to above resting levels following exercise cessation).
http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320633
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008

The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been considered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more recent literature. Previously this phenomenon has been described as a decrement in both arterial oxygen partial pressure (PaO₂) and oxy-haemoglobin saturation (SaO₂or SpO₂) with, particularly important for PaO₂, a lack of or inappropriate correction made for the change in body temperature during intense exercise. The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with an offset of approximately 1.3ºC, and were considered much more appropriate and relevant indicators of thermal changes during exercise. As an extension of the initial work active muscle temperature (vastus lateralis) was measured during the exercise test, demonstrating a significantly lower resting temperature than the oft-reported “core” temperatures (rectal and oesophageal) as well as a significantly greater increase in temperature in comparison to all other measurement sites. Overall, the results of this first study indicated that the physiologically relevant temperatures measured at the oesophageal and muscle sites differed markedly to the outdated rectal temperature measurement site and should be used as measures of thermal response when evaluating oxygen loading (oesophageal) or unloading (active muscle). Utilising the definition of EIH as a decrease in PaO₂ of ≥ 10 mmHg, the effect of temperature correcting PaO₂ was evaluated in the second study. Arterial blood gases measured simultaneously to the temperature measurements during the incremental exercise test were adjusted for the temperature changes at each site (every 1ºC increase in temperature will increase a PaO₂ value by ~5 mmHg). Whilst uncorrected PaO₂ values indicated an almost 100% prevalence of EIH in this group, oesophageal temperature corrected PaO₂ values decreased this prevalence to ~50% while muscle temperature corrections resolved all cases of EIH and demonstrated an HYPEROXAEMIA (i.e. the reverse of the well-established phenomenon) in the majority of subjects. Further investigation of arterial oxygen content during the exercise test indicates that there is no disruption in the delivery of oxygen to the active muscles and therefore any performance decrement should be attributed to another mechanism. Whilst the phenomenon of EIH is determined by the definition applied and the use of temperature corrections in the case of PaO₂, its reproducibility in a test-retest situation had not previously been determined. Utilising a subset of previously tested subjects, the reproducibility of both temperature and PaO₂ were determined with results indicating that the blood gas response was highly reproducible, especially the minimum PaO₂ value noted during each exercise test. However, comparing a more statistically relevant definition of a change in PaO₂ of ± 2 standard deviations from the mean resting PaO₂ to the previous delimiter of 10 mmHg indicated a lesser reproducibility of the prevalence of EIH. In summary, this thesis exposes the inadequacies of previous research into EIH with regard to the expected reproducibility of the phenomenon and the need to correctly adjust PaO₂ values for exercise-induce hyperthermia as well as demonstrating the difference in thermal responses to acute exercise in physiologically significant areas of the body. Furthermore, previously described correlations between the change in PaO₂ and VO₂ max were not evident in the subjects tested within this thesis, nor was there any indication of a diffusion limitation based on reduced pulmonary capillary transit time (by association with VO₂ max) or pulmonary oedema (rebuked by a rapid return of PaO₂ to above resting levels following exercise cessation).
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008

Indiana University-Purdue University Indianapolis (IUPUI)
Photoacoustic Imaging is a non-invasive optical imaging modality used to image biological tissues. In this method, a pulsating laser illuminates a region of tissues to be imaged, which then generates an acoustic wave due to thermal volume expansion. This wave is then sensed using an acoustic sensor such as a piezoelectric transducer and the resultant signal is converted into an imaging using the back projection algorithm. Since different types of tissues have different photo-acoustic properties, this imaging modality can be used for imaging different types of tissues and bodily organ systems. This study aims at quantifying the process of light conversion into the acoustic signal. Light travels through tissues and gets attenuated (scattered or absorbed) or reflected depending on the optical properties of the tissues. The process of light propagation through tissues is studied using Monte Carlo simulation software which predicts the propagation of light through tissues of various shapes and with different optical properties. This simulation gives the resultant energy distribution due to light absorption and scattering on a voxel by voxel basis. The Monte Carlo code alone is not sufficient to validate the photon propagation. The success of the Monte Carlo code depends on accurate prediction of the optical properties of the tissues. It also depends on accurately depicting tissue boundaries and thus the resolution of the imaging space. Hence, a validation algorithm has been designed so as to recover the optical properties of the tissues which are imaged and to successfully validate the simulation results. The accuracy of the validation code is studied for various optical properties and boundary conditions. The results are then compared and validated with real time images obtained from the photoacoustic scanner. The various parameters for the successful validation of Monte Carlo method are studied and presented. This study is then validated using the algorithm to study the conversion of light to sound. Thus it is a significant step in the quantification of the photoacoustic effect so as to accurately predict tissue properties.