Dissertations / Theses on the topic 'Hypercapnia'
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Jeton, Florine. "Etude du rôle de l’Erythropoïétine et des systèmes de neurotransmission dans la mise en place des réponses ventilatoires à l’hypoxie et à l’hypercapnie." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCD078/document.
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Lors de variations de PO2 et PCO2, différents mécanismes se mettent en place afin demaintenir l’oxygénation des tissus, notamment au niveau du métabolisme et de la ventilation. En casde stimulation hypoxique ou hypercapnique, on observe alors une réponse ventilatoire, caractériséepar une augmentation progressive de la ventilation. Parmi les facteurs qui influencent la réponse àl’hypoxie, on trouve l’érythropoïétine (Epo) qui, en plus de son rôle dans l’érythropoïèse, possèded’autres rôles, notamment au sein du système nerveux central. Cette thèse présente l’étude del’implication de l’Epo et de différents systèmes de neurotransmission dans les réponses ventilatoiresà l’hypoxie (RVH) et à l’hypercapnie (RVHc).Nous avons alors pu mettre en évidence l’implication du NO, du glutamate et de la sérotonine dansla RVH et dans l’acclimatation ventilatoire à une hypoxie prolongée (VAH) chez un modèle de sourisanémique déficient en Epo (Epo-TAgh) et un animal adapté à la vie en altitude, la plateau Pika. Nousavons ensuite étudié l’impact de la déficience en Epo sur la RVHc, et nous avons confirmé que l’Epon’était pas nécessaire à l’obtention de la RVHc, tout en mettant en évidence un rôle de l’Epo sur lepatron ventilatoire et sur l’implication de certaines structures du système nerveux central dans lamise en place de cette réponse. Une étude en parallèle sur les femelles a permis de mettre enévidence que le cycle oestral n’était pas impliqué dans les réponses ventilatoires mais qu’il semble yavoir une interaction entre l’Epo et les hormones sexuelles femelles dans la RVH et la RVHc. Enfin,différentes expériences réalisées lors de collaborations (Chili, Canada) ont permis d’étudier les effetsde l’Epo sur les chémorécepteurs centraux et périphériques dans la mise en place des réponsesventilatoires.In fine, ces différentes expériences ont permis de préciser les différents facteurs impliqués dans lamise en place des réponses ventilatoires à l’hypoxie et à l’hypercapnie, ce qui pourrait aider par lasuite à mieux comprendre les modifications respiratoires induites par des pathologiques liées àl’anémie ou l’exposition prolongée à l’altitudeWhen PO2 and PCO2 are modified, various mechanisms are being established to maintaintissue oxygenation, such as ventilation and metabolism adaptations. In case of hypoxia orhypercapnia stimulation, we observed a ventilatory response, characterized by an increase in minuteventilation. Among the factors involved in the hypoxic response, Epo plays a key role. In addition toits role in erythropoiesis, Epo has other functions, especially in the central nervous system. Thisthesis presents the study of Epo involvement in the ventilatory responses to hypoxia (HVR) andhypercapnia (HcVR).We demonstrate the involvement of NO, glutamate and serotonin in the HVR and in acclimatizationto sustained hypoxia (VAH) in Epo deficient mice (Epo-TAgh) and in an animal adapted to highaltitude, the plateau Pika. Then we studied the impact of Epo-deficiency on HcVR and confirmed thatEpo is not mandatory to obtained HcVR but we demonstrate that Epo can modulate the ventilatorypattern and central nervous system structures involvement in this response. During this study, wealso demonstrate that in female mice, estrous cycle is not involved in HVR or HcVR but it seems thatthere is an interaction between Epo and female sexual hormones in these responses. Finally, someexperiments in collaboration with different countries (Chile, Canada) allowed us to study the effectsof Epo on peripheral and central chemoreceptors during HVR and HcVR.In fine, these experiments allows us to specify the factors involved in ventilatory responses tohypoxia and hypercapnia, which could be helpful to better understand respiratory pathologies suchas anemia or pathologies associated with high altitude
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Wang, Zhen. "Adjunctive therapies in a clinical revelant ovine model of septic shock." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210196.
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Sepsis has been defined as a systemic response to an infection. With an incidence of 3 per 1000 population per year or about 750 000 cases a year, this syndrome ranks as the 10th leading cause of death in the United States (1). Increasing severity of sepsis correlates with increasing mortality, which rises from 30-40% for severe sepsis up to 40-60% for septic shock. This thesis examines the effectiveness of adjunctive therapies, including activated protein C, hypercapnia and acidosis, and sodium selenite, in a clinically relevant ovine model of septic shock. The results from these studies can provide valuable information for future clinical trials on sepsis.This thesis is divided into four sections: 1) sepsis overview; 2) an autologous fecal peritonitis model in sheep and its evaluation; 3) the series of studies on adjunctive therapeutics; and 4) ongoing studies and future perspective.
In the first section, a broad overview gives a rough introduction to delineate many aspects of sepsis syndrome such as terminology, etiology, epidemiology, pathophysiology and current guidelines for management. Hemodynamics in sepsis are especially elaborated since these are major observations throughout the studies presented later.
In the second section, the general characteristics of the sepsis models used in this thesis are elucidated. Data on hemodynamics, lung mechanics, gas exchange, etc. are presented to feature the ovine peritonitis model. The results of laboratory examinations for hematology, coagulation, bacteriology, biochemistry and hormonology are also presented. And then, I review currently used sepsis models with regards to their advantages and disadvantages.
The third section discusses three studies with their objectives, the methods used, the major findings, and the potential clinical implications.
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1) Beneficial effects of recombinant human activated protein C in experimental septic shock. Activated protein C has a multitude of beneficial effects in severe sepsis and septic shock, including anti-inflammation, anti-coagulation, profibrinolysis, anti-apoptosis and endothelial protection. A clinical Phase III trial demonstrated that the administration of recombinant human activated protein C improved survival in patients with severe sepsis. However, doubts on the protective effects of activated protein C have persisted and been refueled by the recently published negative trials in less severely ill patients and in children. In the light of these ambiguities and uncertainties, we reinvestigated the effects of activated protein C in experimental septic shock.
2) Acute hypercapnia improves indices of tissue oxygenation more than dobutamine in septic shock. Hepercapnia has been found to possess beneficial effects in diverse acute inflammatory states independent of protective lung mechanics. To prove the hypothesis that acute hypercapnia has similar or superior hemodynamic effects to those of a dobutamine infusion, which may be particularly relevant in the presence of hemodynamic instability associated with respiratory failure, we investigated the effects of hypercapnia, which induced by inspiring extrinsic carbon dioxide in experimental septic shock.
3) High bolus dose of sodium selenite prolongs survival in an ovine model of septic shock. Selenite has both pro- and anti-oxidant effects. The administration of high dose sodium selenite may improve survival in septic shock patients. The benefit may be greater with the administration of a bolus (to achieve higher concentrations) rather than a continuous infusion. To test this hypothesis, we examined the effects of a high dose bolus administration of sodium selenite in experimental septic shock.
The fourth and final section talks about currently ongoing studies and offers some perspective on future direction.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
3
Bailey, Elizabeth Fiona. "Breathing behavior during speech production in hypercapnia." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282812.
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This investigation was designed to examine speech production, the motion of the chest wall, and breathing-related perceptions under a condition of heightened respiratory drive. Ten healthy young men were studied during spontaneous breathing and during speaking in three gas conditions: room air, air delivered from a pressurized tank, and a gas mixture high in carbon dioxide (7% CO₂) delivered from a pressurized tank. Magnetometers that transduced diameter changes of the rib cage and abdomen were used to study chest wall motion. Subjects also reported their breathing-related perceptions. Results indicate that chest wall behavior during spontaneous breathing and speaking did not differ between room-air and tank-air conditions, but differed substantially in the high-CO₂ condition. In the high-CO₂ condition, spontaneous breathing and speaking usually were characterized by larger lung volumes, larger rib cage volumes, higher breathing rates, longer expiratory times, and higher expiratory flows than in the two air conditions. Further, speaking in high-CO₂ was characterized by shorter speech duration, fewer syllables per breath group, and greater average lung volume expenditure per syllable compared to speaking in air. In high-CO₂, subjects reported a range of breathing-related percepts including "breathlessness," "effortful breathing," and "gasping for air." Without exception, speaking in high-CO₂ was judged by the subjects to be more difficult than breathing in high-CO₂.
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Tansley, John Guion. "Human ventilatory responses to prolonged hypoxia and hypercapnia." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363954.
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Binks, Andrew Paul. "Breathlessness and the pattern of breathing." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263019.
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Taylor, John Andrew 1960. "RESPIRATORY CHEMOSENSITIVITY IN SYNCHRONIZED SWIMMERS AND SWIM-TRAINED WOMEN." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276444.
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Jarsky, Tim M. "The effects of hypoxia and hypercapnia on hamster activity rhythms." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0009/MQ29356.pdf.
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Miller, Scott. "Cardiac Responses to Carbon Dioxide in Developing Zebrafish (Danio rerio)." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24210.
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The ontogeny of carbon dioxide (CO2) sensing in zebrafish (Danio rerio) has not been studied. In this thesis, CO2-mediated increases in heart rate were used to gauge the capacity of zebrafish larvae to sense CO2. CO2 is thought to be sensed through neuroepithelial cells (NECs), which are homologous to mammalian carotid body glomus cells. Owing to its role in facilitating intracellular acidification during exposure to hypercapnia, it was hypothesized that carbonic anhydrase (CA) is involved in CO2 sensing, and that inhibition of CA would blunt the downstream responses. The cardiac response to hypercapnia (0.75% CO2) was reduced in fish exposed to acetazolamide, a CA inhibitor, and in fish experiencing CA knockdown. Based on pharmacological evidence using β-adrenergic receptor (ß-AR) antagonists, and confirmed by β1AR gene knockdown, the efferent limb of the reflex tachycardia accompanying hypercapnia is probably mediated by sympathetic adrenergic neurons interacting with cardiac β1 receptors.
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Nanagas, Vivian C. "Clamping of Intracellular pH in Neurons from Neonatal Rat Brainstem during Hypercapnia." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1246393988.
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Martin, James. "The Responses of Blue Crabs (Callinectes sapidus) to Hypoxia/Hypercapnia in Freshwater." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1847.
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The present research examined respiratory responses of blue crabs to long term (4, 13, and 21 days) hypercapnic hypoxia in freshwater at 23 C. Hypoxic conditions (50-60 & 75-85 mmHg O2) were induced by allowing the crabs to consume their oxygen supply, resulting in a hypercapnic induced decrease in pH that remained through the exposure. Postbranchial hemolymph responses to hypoxia/hypercapnia in freshwater demonstrate decreases in PO2, increases in PCO2, and decreases in pH. Lactate levels decreased over time, but hemocyanin concentration was highly variable with no trends. PH, lactate, and hemocyanin observations also demonstrated high variability and a variety of different responses in individual crabs. There was no evidence of improving oxygen transport abilities. Despite varying responses high mortality rates were observed. The high mortality rate suggests blue crabs are not able to survive the multiple stress of hypoxia/hypercapnia along with the stress of living in freshwater. The mortality rates observed are much greater than previous blue crab hypoxic studies in saltwater. Elevated mortality may result from a failure of oxygen transport, acid-base balance or ion regulation.
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Abdallah, Sara. "Role of Intracellular Ca2+ and pH in CO2/pH Chemosensitivity in Neuroepithelial Cells of the Zebrafish (Danio rerio) Gill Filament." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23775.
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Neuroepithelial cells (NECs) of the zebrafish gill filament have been previously identified as bimodal O2 and CO2/H+ sensors that depolarize in response to chemostimuli via inhibition of background K+ channels. To further elucidate the signaling pathway underlying CO2/H+ chemoreception in the NECs we employed microspectrofluorometric techniques to examine the effects of hypercapnia on [Ca2+]i and pHi. NECs increased their [Ca2+]i in response to acidic hypercapnia (5% CO2, pH 6.6) and isocapnic acidosis (normocapnia, pH 6.6), but not to isohydric hypercapnia (5% CO2, pH 7.8). The acid- induced increase in [Ca2+]i persisted in the absence of extracellular Ca2+, and Ca2+ channel blockers (Cd2+, Ni2+ and nifedipine). NECs exhibited a rapid and reversible drop in pHi in response to acidic hypercapnia and isohydric hypercapnia. Isocapnic acidosis also induced intracellular acidification within NECs, but it was less severe than the drop in pHi elicited by acidic hypercapnia and isohydric hypercapnia. The rate and magnitude of intracellular acidification was reduced by the CA-inhibitor, acetazolamide, without effect on the acid-induced increase in [Ca2+]i. Acetate was used to investigate the relationship between pHi and [Ca2+]i. Acetate induced intracellular acidification without augmentation of [Ca2+]i. The results of this thesis demonstrate that (1) extracellular acidification, but not CO2, is critical to the hypercapnia-induced increase in [Ca2+]i (2) the increase in [Ca2+]i is independent of the drop in pHi (3) the increase in [Ca2+]i is not mediated by the influx of Ca2+ across the plasma membrane.
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Accili, Eric Anthony. "The effects of systematic hypercapnia on the hindlimb perfusion pressures of acute spinal cats." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26158.
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Normal levels of CO₂ are responsible for the maintenance of approximately 30% of sympathetic neurogenic vascular tone in intact cats. The central medullary chemoreceptors have been implicated as the major source of this CO₂ dependent neurogenic vascular tone. However, it is possible that spinal cord CO₂ sensitivity could also have mediated a portion of neurogenic vascular tone.
Cats with acute and chronic spinal transections can maintain near normal levels of systemic arterial blood pressure, and show cardiovascular and sympathetic reflex changes in response to a variety of stimuli.
Thus, it seemed likely that the acute spinal cat could exhibit the spinal component of CO₂ mediated sympathetic neurogenic vascular tone. Therefore the effects of systemic CO₂ increases on the perfusion pressures of vascularly isolated hindlimbs autoperfused at constant flow (as an indication of vascular resistance and sympathetic vascular tone) were studied in the acute cervical spinal cat. The contributions of the lumbar sympathetic system and the adrenal glands to perfusion pressure responses to CO₂ were evaluated.
Experiments were carried out in mongrel cats with acute cervical (C2) transections. Each cat had one leg denervated by cutting and stripping the lumbar sympathetic chain from L₁-L₇. In all cats each hindlimb was vascularly isolated and perfused with blood taken from the abdominal aorta. Bilateral adrenalectomy was performed on 8 animals.
CO₂ administration for 5 minutes resulted in biphasic increases in the perfusion pressures of both legs which were designated peak1 (P1) and peak2 (P2). Increasing PCO₂ from 16 to 38mm Hg, and from 16 to 62mm Hg resulted in significant P1 and P2 responses of the innervated leg. This also resulted in a significant P2 response, and an observable but insignificant P1 response, of the denervated leg. Adrenalectomy reduced P1 and P2 responses of the innervated leg, and abolished the P1 response and reduced the P2 response of the denervated leg. In non-adrenalectomized cats increasing PCO₂ also resulted in a significant increase in systemic arterial pressure (SAP) with no changes in heart rate (HR). In adrenalectomized cats increasing PCO₂ resulted in an observable but non-significant increase in SAP and a significant decrease in HR.
These results suggested that:
1) The P1 response was primarily a sympathetic neurogenic response to increased CO₂.
2) The P2 response was primarily a hormonal response to CO₂ in the denervated leg, and a combination of hormonal and sympathetic neurogenic responses to CO₂ in the innervated leg.
3) The adrenal glands were mostly involved in the P2 response to CO₂, but possibly had a small role in the P1 response.
4) Other non-adrenal vasoconstrictor hormones may have played a role in the P2 response to C0₂.
5) Likely, CO₂ initially activated the sympathetic system to directly increase neurogenic tone, perhaps by stimulating sympathetic afferent or efferent neurons, or hypothetical spinal chemosensitive regions. Progressively the adrenal and possibly other unidentified vasoconstrictor hormone systems became activated, either directly by CO₂ or indirectly by CO₂ mediated sympathetic activation. These hormone systems may have also played a role in CO₂ mediated maintenance of vascular tone.Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
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Kunert, Emma. "The Role of Carbonic Anhydrase in Cardiorespiratory Responses to CO2 in Zebrafish (Danio rerio)." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42098.
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Adaptation to environmental fluctuations, through sensing and appropriate physiological responses, is crucial to homeostasis. Neuroepithelial cells (NECs) are putative chemoreceptors resembling mammalian Type I (glomus) cells. They have been shown to respond in vitro to changes in O2, CO2, NH3 and pH. Cytosolic carbonic anhydrase (Ca17a) is thought to be involved in CO2 sensing owing to its presence in NECs. A mutant line of zebrafish (Danio rerio) lacking functional Ca17a was generated using CRISPR/Cas9 technology and used to assess the role of Ca17a in initiating the cardiorespiratory responses to elevated CO2 (hypercapnia). Unfortunately, the homozygous knockout mutants (ca17a-/-) did not survive longer than ~12-14 days post fertilization (dpf), restricting experiments to early developmental stages (4-8 dpf). Changes in ventilation (fV) and cardiac (fH) frequency in response to hypercapnia (1% CO2) in wild type (ca17a+/+), heterozygous (ca17a+/-) and ca17a-/- fish were used to investigate Ca17a-dependent CO2 sensing and downstream signalling. Wild type fish exhibited hyperventilation during hypercapnia as indicated by an increase in fV. In the ca17a-/- fish, the hyperventilatory response was attenuated markedly, but only at 8 dpf. Hypercapnic tachycardia was observed for all genotypes and did not appear to be influenced by the absence of Ca17a. Interestingly, ca17a-/- fish exhibited a significantly reduced resting fH¬. This effect of knockout became more pronounced as the fish aged. Anesthesia did not contribute to the decreased fH in the ca17a-/- fish, nor did changes in cardiac adrenergic or cholinergic tone, which were probed using propranolol (-adrenergic receptor blocker) or atropine (muscarinic receptor blocker). The decrease in resting fH was prevented (“rescued”) when ca17a-/- embryos were injected with ca17a mRNA. Collectively, the results of this thesis support a role for Ca17a in promoting hyperventilation during hypercapnia in larval zebrafish and suggest a previously unrecognized role for Ca17a in determining resting heart rate.
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Croft, Quentin. "Human responses to simulated high altitude." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711614.
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Turner, Mark John. "The effects of hypercapnia on CFTR-dependent HCOb3p-s secretion in human airway epithelia." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2876.
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Hypercapnia is clinically defined as an arterial blood partial pressure of CO2 of above 40mm Hg and is a symptom of chronic lung disease. In renal epithelia, hypercapnia can reduce agonist-stimulated cAMP levels and impair regulation of cAMP-dependent ion transporters. In the airways, elevations in intracellular cAMP in serous cells of the submucosal glands, activates CFTR-mediated HCO3- and fluid secretion, which contributes to airway surface liquid homeostasis. The aim of the current work was to investigate the effects of both acute and chronic hypercapnia on cAMP-regulated ion and fluid transport in Calu-3 cells, a model of human serous cells. Acute hypercapnia significantly reduced both forskolin-stimulated elevations in intracellular cAMP and forskolin-stimulated increase in short-circuit current, suggesting CO2 reduced cAMP-regulated, CFTR-dependent anion secretion. Stimulation of Calu-3 cells with cAMP agonists induced a reversible intracellular acidification that was a result of CFTR-dependent HCO3- secretion. In acute hypercapnia, this intracellular acidification was significantly augmented yet neither CFTR-dependent HCO3- efflux, nor NBC-dependent HCO3- influx, were found to be CO2-sensitive. However, ouabain blocked the augmentation induced by hypercapnia implicating the Na+/K+-ATPase in mediating the effects of raised CO2 on cAMP-mediated cytosolic acidification. In addition, both BAPTA-AM and the phospholipase C inhibitor, U77312, also blocked the effect of hypercapnia, implying a role for PLC-regulated Ca2+ mobilization in the pH response to hypercapnia. Although addition of exogenous ATP in normocapnia mimicked the effect of hypercapnia, there was little evidence that CO2-induced ATP release from Calu-3 cells, which therefore suggests the effect of hypercapnia is not due to ATP/Ca2+ signalling via purinergic receptors. Exposure of Calu-3 cells to 24 hours hypercapnia caused a significant reduction in the volume of fluid secreted but did not affect the HCO3- or mucus content of this secreted fluid. These data suggest that transporters involved in regulating the volume of secreted fluid have differential CO2 sensitivity compared to transporters involved in regulating its composition. These findings reveal that both acute and chronic hypercapnia affected ion and fluid transport in human airway epithelial cells, and suggests hypercapnia could have pronounced effects on the properties of the airway surface liquid which would be predicted to have important consequences for the innate defence mechanisms of the lungs.
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Bartlett, Kate. "Changes in Cortical Tissue Oxygenation in rodent somatosensory cortex produced by sensory stimuli and hypercapnia." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500531.
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Hypes, Sandra R. "Sub-Lethal Effects of Hypoxia/Hypercapnia on Callinectes Sapidus in the York River Estuary, Virginia." VCU Scholars Compass, 1999. http://scholarscompass.vcu.edu/etd/1346.
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This research examined effects of hypoxic environments on blue crabs, Callinectes sapidus in an estuarine environment. Hypoxic conditions were treated as a multiple stressor involving low dissolved oxygen (D.O.), increased carbon dioxide (hypercapnia), and low pH concurrently. The objectives were to: 1) identify hypoxiahypercapnia by monitoring D.O. and pH as an indicator of hypercapnia in shallow regions of the York River, 2) measure blue crab abundance, and 3) describe blue crab responses to hypoxiahypercapnia via field work at Taskinas Creek and lab measurements of respiration. Ambient D.O. and pH were positively correlated in the Taskinas Creek and York River sites (r= .73). Crab abundance (CPUE) was not significantly different among D.O. and pH ranges. It was concluded that hemolymph blood lactate concentration was not considered a good in situ biomarker for exposure to hypoxickypercapnic conditions. Oxygen uptake was not significantly different between normoxic and hypoxic conditions but was significantly affected by pH.
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Tinworth, Kellie. "Arousal, Sleep and Cardiovascular Responses to Intermittent Hypercapnic Hypoxia in Piglets." Thesis, The University of Sydney, 2003. http://hdl.handle.net/2123/1116.
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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.
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Tinworth, Kellie. "Arousal, Sleep and Cardiovascular Responses to Intermittent Hypercapnic Hypoxia in Piglets." University of Sydney, 2003. http://hdl.handle.net/2123/1116.
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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.
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Marschand, Rachel E. "Effects of Airway Pressure, Hypercapnia, and Hypoxia on Pulmonary Vagal Afferents in the Alligator (Alligator Misssissippiensis)." Thesis, University of North Texas, 2013. https://digital.library.unt.edu/ark:/67531/metadc407750/.
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The American alligator (Alligator mississippiensis) is an aquatic diving reptile with a periodic breathing pattern. Previous work has identified pulmonary stretch receptors (PSR), both rapidly- and slowly-adapting, and intrapulmonary chemoreceptors (IPCs) that modulate breathing patterns in alligators. The purpose of the present study was to identify the effects of prolonged lung inflation and deflation (simulated dives) on PSR and/or IPC firing characteristics in the alligator. The effects of airway pressure, hypercapnia, and hypoxia on dynamic and static responses of pulmonary stretch receptors (PSR) were studied in juvenile alligators (mean mass = 246 g) at 24°C. Receptor activity appeared to be a mixture of slowly-adapting PSRs (SARs) and rapidly-adapting PSRs (RARs) with varying thresholds and degrees of adaptation, but no CO2 sensitivity. Dives were simulated in order to character receptor activity before, during, and after prolonged periods of lung inflation and deflation. Some stretch receptors showed a change in dynamic response, exhibiting inhibition for several breaths after 1 min of lung inflation, but were unaffected by prolonged deflation. For SAR, the post-dive inhibition was inhibited by CO2 and hypoxia alone. These airway stretch receptors may be involved in recovery of breathing patterns and lung volume during pre- and post-diving behavior and apneic periods in diving reptiles. These results suggest that inhibition of PSR firing following prolonged inflation may promote post-dive ventilation in alligators.
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Elhossaini, Hawraa. "Proliferation and Primitivity of Hematopoietic Progenitor Cells in Hypoxic Hypercapnic Conditions." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/30010.
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This thesis aims to improve the in vitro cultivation of hematopoietic stem cells (HSCs) by exploring the effects of various biophysical and biochemical factors. The study uses KG-1a cells as a model for HSCs and evaluates the impact of different O2/CO2 conditions on apoptosis, proliferation, and primitivity. Additionally, the effect of differently-treated cuttlefish bone (CB) on mouse bone marrow hematopoietic cells is examined. The results show that combining hypoxia and hypercapnia is more effective in maintaining CD34+ cell count, survival, and primitivity compared to other gas combinations and control conditions. The study also found that crushed cuttlefish bone supports cell proliferation, viability, and primitivity, most likely through the presence of CaCO3 microparticles and the production of VEGF and TGF-1. These findings have the potential to improve engraftment success rates in medical treatments and enhance the reconstitution of a healthy hematopoietic system in patients.
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Hammer, Karen M. "Acid-base regulation and metabolite responses in shallow- and deep-living marine invertebrates during environmental hypercapnia." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for biologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-19773.
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Global warming is considered to be the most adverse consequence from the increasing anthropogenic emissions of CO2. However, in the marine environment additional problems related to the elevated levels atmospheric CO2 may arise; the increased amount of CO2 absorbed by the oceans may lead to a moderate, but consistent and global reduction in seawater pH due to the acidifying effect of CO2, a phenomenon referred to as ocean acidification. Another potential problem may occur as a result of sub-seabed storage of anthropogenic CO2, a disposal alternative introduced by the gas industry to mitigate CO2 emissions to the atmosphere. Leakage from such storage sites could potentially cause a relatively local, but extreme acidification of the seawater near the leakage site. Both scenarios may create unfavourable conditions for marine organisms, and previous studies have reported that environmental hypercapnia (elevated pCO2) may affect an array of physiological processes in marine organisms such as acid-base status and metabolic rate. Deep-living animals are considered to be particularly vulnerable to environmental hypercapnia due to their low metabolic rate and poor ability to counteract effects of environmental stressors. To predict the possible outcome of the two scenarios described above it is important to understand the physiological mechanisms that marine organisms apply to handle the CO2 stress. During conditions of elevated seawater pCO2, the charge neutral CO2 molecules permeate biological membranes and react with water in the body fluids resulting in the net formation of HCO3- and H+. Thus, the primary effect of elevated pCO2 is induction of body fluid acidosis. Acid-base regulation during acidosis is generally mediated by buffering compounds as well as acid elimination through direct removal of hydrogen ions (H+) and/or accumulation of buffering bicarbonate ions (HCO3-). In the current thesis the deep-sea bivalve Acesta excavata, the green shore crab Carcinus maenas, and the deep-water prawn Pandalus borealis were exposed to elevated seawater levels of pCO2. The purpose was to study the responses of the different species to elevated pCO2 and to compare the capacity of shallow- and deep-living animals to counteract CO2-induced effects. To meet these objectives changes in acid-base relevant parameters (pH, pCO2, [HCO3-]) and metabolic rate was studied in all three species, while gene expression and activity of ion regulating proteins as well as changes in the metabolome were determined in C. maenas alone. Calcifying animals, such as bivalves, have been suggested to utilise HCO3- from the calcium carbonate shell to buffer acidosis. However, this buffering strategy may be restricted to closed systems such as during shell closure. Indeed, the findings in the present thesis indicate that shell dissolution does not occur in the deep-living bivalve A. excavata in response to CO2-induced acidosis. Consequently, A. excavata does not seem to be able to compensate extra- or intracellular acidosis in response to severe environmental hypercapnia, and experiences a drop in metabolic rate most likely induced by low body fluid pH. However, this species displays a relatively high nonbicarbonate buffering capacity, and may therefore be able to tolerate more moderate levels of CO2 exposure than that experienced in the present study. In decapod crustaceans extracellular pH-regulation occurs in the posterior gills by electroneutral ion exchange between the extracellular fluids and the surrounding seawater. The shore crab C. maenas was able to partially compensate extracellular acidosis by accumulating relatively high levels of HCO3- in response to elevated pCO2, and the degree of compensation was dependent on the level of CO2 exposure. The results from the present thesis suggest that this species can compensate acidosis without substantially increasing the acid-base regulatory capacity of the branchial ion transporting proteins. Surprisingly, the deep-water prawn Pandalus borealis exhibited similar abilities as the shore crab to counteract extracellular acidosis induced by elevated pCO2. This was achieved by increasing the extracellular concentration of HCO3- to a similar degree as C. maenas. The findings indicate that this species display similar acid-base regulatory capacities as shallow-living decapods, thus nuancing the picture of the compensating capacities of deep-living animals. Acid-base regulation in both decapod species was achieved without affecting the osmolality of the extracellular fluid. This is in contrast to what has been reported for subtidal decapod crabs. The metabolic rate was not significantly affected in any of the two species, possibly due to their ability to maintain extracellular pH close to normal values. While acid-base regulation in response to CO2-induced acidosis has received increased scientific attention, only a very few studies have investigated responses of the metabolome to elevated pCO2. 1H-NMR metabolomics revealed that in the green shore crab CO2 exposure induces a shift in the metabolic fingerprint in both hemolymph and extracts of gills and leg muscle. The shift is not the result of changes in metabolites involved in energy metabolism, as could be expected. Rather, it is due to a general decrease in the concentration of metabolites, particularly of important osmolytes such as the amino acids proline and glycine. The observed changes were most prominent after prolonged exposure, suggesting an exhaustive response rather than an active, compensatory mechanism. The results indicate that in response to elevated pCO2 shore crabs experience symptoms resembling those of animals acclimated to condtions of reduced salinity. This may possibly suggests a disturbance of intracellular isoosmotic regulation. The present thesis indicates that A. excavata would be highly, and possibly permanently affected by severe CO2 exposure associated with CO2 leakage, while both the intertidal and deep-living decapods could tolerate relatively prolonged periods of quite severe hypercapnic conditions.
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Hamad, Mouna. "Toward an Understanding of How Hypercapnia Affects Apoptosis in Human Promyeloblasts in 3D Suspension Culture Systems." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/16960.
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Stem cells have more recently attracted interest in scientific research and their use is increasingly developing in many therapeutic applications. A great deal of cell-based work is conducted at 5% CO2 concentration and is predominantly cultured on two-dimensional surfaces. These methods are straightforward and of low economic costs but do not necessarily replicate the microenvironment; also, evidence to provide justification for selecting this specific concentration of CO2 in hematopoietic progenitor cell (KG-1a) proliferation studies is lacking. Our work herein pursues to prove the following hypotheses: (a) Hypercapnia decelerates proliferation rate but increases overall expansion of KG-1a cells without disturbing cell surface integrity, (b) Apoptosis of KG-1a cells is delayed under the effect of hypercapnia in both 2D and 3D culture systems, (c) KG-1a cells can successfully proliferate within a 3D bioreactor system to yield higher cell concentrations than 2D systems. This work was successful in proving that in both 2D and 3D culture systems, hypercapnia decelerates proliferation rate but increases overall expansion of KG-1a without disturbing cell surface integrity in comparison to hypocapnic and control populations. Also, we established that the apoptotic capacity of these KG-1a cells is delayed under the effect of hypercapnia in both 2D and 3D culture systems. And finally, this work has demonstrated that KG-1a cells can successfully proliferate within a 3D bioreactor system to yield comparable cell concentrations to traditional 2D systems. This study has succeeded in adding to the current body of knowledge that exists on hematopoietic stem cell expansion and it may potentially provide the foundation to enhancing proliferation systems of hematopoietic stem cells and therefore contribute to resolving numerous diseases.
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Dodd, Graham Alan Andrew. "The effects of acute and chronic hypercapnia upon ventilation and acid-base status in the pekin duck." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/27417.
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In this study, awake Pekin ducks (Anas platyrhynchos) were exposed to periods of acute and chronic hypercapnia (0.05 F₁CO₂). Measurements were made of ventilation and acid-base status in both adult and juvenile male ducks as well as in adult female ducks. All Pekin ducks, regardless of age or sex, responded acutely to inspired CO₂ with a marked hypercapnic-hyperpnea. Inhalation of CO₂ resulted in a significant increase in arterial CO₂ tension (PaCO₂) and decrease in arterial pH (pHa). The increase (3 times (x)) in minute ventilation (V[sub E]), while primarily a function of an increase (2x) in tidal volume (V[sub T]), also involved an increase (1.5x) in breathing frequency (f[sub b]).
The chronic responses of ducks to inspired CO₂, however, did differ depending upon the sex of the animal. In male ducks, the initial increase observed in V[sub E]during the first 20 minutes was reduced by 50% after 300 minutes. This partial recovery in V[sub E]resulted entirely from the complete return of f[sub b] to its control levels as V[sub T]remained both elevated and constant throughout the period of hypercapnia. In addition, the male ducks also demonstrated a significant recovery (50%) in pHa, a change that was paradoxical to the concomitant increase measured in PaCO₂. While a change in strong ion difference (SID) was not detected, the accompanying rise in calculated arterial [HCO₃⁺] suggested that metabolic compensatory processes must have alleviated the initial respiratory acidosis. The rate of metabolic compensation seen in the ducks of this study exceeds that reported for any other air-breathing vertebrate. Female ducks, on the other hand, maintained the initial increase in V[sub E]and decrease in pHa throughout the period of CO₂ exposure. The reasons for this remain unclear although it is speculated that the metabolic demands of eggshell formation may have limited the capacity of these birds to mobilize further HCO₃⁻ stores.
Differences in the changes which occurred in f[sub b], V[sub T], pH and P[sub CO₂] in male and female ducks during chronic CO₂ exposure strongly suggest that the changes in f[sub b] were a singular function of changes in pHa ([H⁺]) while changes in VT were primarily a function of changes in PaCO₂. Denervation of peripheral chemoreceptors appeared to have little effect upon the overall ventilatory responses to either acute or chronic hypercapnia, suggesting that central chemoreceptors must have been predominantly responsible for the ventilatory responses observed during this study.Science, Faculty of
Zoology, Department of
Graduate
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Najarian, Taline. "Hypercapnia-induced, potassium channel and prostaglandin dependent modulation of endothelial constitutive nitric oxide synthase in neonatal brain." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0034/MQ64414.pdf.
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Buchbinder, Benno Andreas [Verfasser]. "Impact of hypercapnia on alveolar Na+-transport : Establishing a system for ENaC-protein detection / Benno Andreas Buchbinder." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/1065478976/34.
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Ratnavadivel, Rajeev, and rajeev ratnavadivel@health sa gov au. "The Importance of Non-Anatomical Factors in the Pathogenesis of Obstructive Sleep Apnoea." Flinders University. Medicine, 2009. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20090901.162141.
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Obstructive sleep apnoea (OSA) is a common condition characterized by recurrent complete and partial upper airway obstruction. OSA sufferers have been shown to have a significantly smaller upper airway lumen compared to non-OSA sufferers. However, non-anatomical factors of sleep stage, arousability and neuromechanical responses to airway occlusion and chemosensitivity are likely to play a significant part in influencing OSA severity across the night. An exploration of these non-anatomical factors forms the basis for the experiments in this thesis.
In the first experimental chapter presented in this thesis, a detailed retrospective epoch by epoch analysis of nocturnal polysomnography in 253 patients referred to a clinical sleep service was performed to examine differences in sleep apnoea severity and arousal indices across the different stages of sleep, while controlling for posture. Both patients with and without OSA demonstrated significant reductions in respiratory and arousal event frequencies from stage 1 to 4 with intermediate frequencies in REM sleep. Lateral posture was also associated with significant improvements in OSA and arousal frequencies, with an effect size comparable to that of sleep stage. The majority of patients showed significant reductions in OSA severity during slow wave sleep. In non-REM sleep, there was a strong correlation between OSA severity and arousal frequency. These results confirm in a large group of patients, a strong sleep stage dependence of both OSA and arousal frequencies.
The second study in this thesis explores the development of a CO2 stabilising or clamp device to enable the provision of positive airway pressure, and by proportional rebreathing, the maintenance of relatively constant end-tidal CO2 despite significant hyperventilation. Healthy volunteers performed brief periods of significant voluntary hyperventilation at 2 levels of CPAP with the rebreathing function off and with active CO2 clamping in randomized order. Compared to CPAP alone, the device substantially attenuated hypocapnia associated with hyperventilation.
The third study of the thesis was designed to investigate if increasing and stabilizing end-tidal CO2 could improve obstructive breathing patterns during sleep. 10 patients with severe OSA underwent rapid CPAP dialdown from therapeutic to a sub-therapeutic level to experimentally induce acute, partial upper airway obstruction over 2 minute periods repeated throughout the night. The CO2 clamp device developed and validated in Study 2 was used to determine whether during periods of partial upper airway obstruction with severe flow limitation, (1) increased end-tidal CO2 resulted in improved airflow and ventilation and (2) clamping end-tidal CO2 lessened post-arousal ventilatory undershoot. Three conditions were studied in random order: no clamping of CO2, clamping of end-tidal CO2 3-4 mmHg above eucapnic levels during the pre-dialdown baseline period only, and clamping of CO2 above eucapnia during both baseline and dialdown periods. Elevated CO2 in the baseline period alone or in the baseline and dialdown periods together resulted in significantly higher peak inspiratory flows and ventilation compared to the no clamp condition. Breath-by-breath analysis immediately pre- and post-arousal showed higher end-tidal CO2 despite hyperventilation immediately post-arousal and attenuation of ventilatory undershoot in CO2 versus non-CO2 clamped conditions. These results support that modulation of ventilatory drive by changes in pre- and post-arousal CO2 are likely to importantly influence upper airway and ventilatory stability in OSA.
The fourth study was designed to explore several possible pathophysiological mechanisms whereby obstructive sleep apnoea is improved in stages 3 & 4 (slow wave) versus stage 2 sleep. 10 patients with severe OSA who demonstrated significant reductions in OSA frequency during slow wave sleep on diagnostic investigation were studied. Patients underwent rapid dialdowns from therapeutic CPAP to 3 different pre-determined sub-therapeutic pressures to induce partial airway obstruction and complete airway occlusions in a randomised sequence during the night in both stage 2 and slow wave sleep. Partial airway obstructions and complete occlusions were maintained until arousal occurred or until 2 minutes had elapsed, whichever came first. After airway occlusions, time to arousal, peak pre-arousal negative epiglottic pressure and the rate of ventilatory drive augmentation were significantly greater, suggesting a higher arousal threshold and ventilatory responsiveness to respiratory stimuli during slow wave compared to stage 2 sleep. Post dialdowns, the likelihood of arousal was lower with less severe dialdowns and in slow wave compared to stage 2 sleep. Respiratory drive measured by epiglottic pressure progressively increased post-dialdown, but did not translate into increases in peak flow or ventilation pre-arousal and was not different between sleep stages. These data suggest that while arousal time and propensity following respiratory challenge are altered by sleep depth, there is little evidence to support that upper airway and ventilatory compensation responses to respiratory load are fundamentally improved in slow wave compared to stage 2 sleep.
In summary, sleep stage, arousal threshold and chemical drive appear to strongly influence upper airway and ventilatory stability in OSA and are suggestive of important non-anatomical pathogenic mechanisms in OSA.
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Fehsenfeld, Sandra. "Linking acid-base balance with nitrogen regulation in the decapod crustacean, Carcinus maenas." Comparative Biochemistry and Physiology, Part A, 2013. http://hdl.handle.net/1993/30977.
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As one of the most successful invasive species in the marine environment around the globe, the green crab Carcinus maenas possesses efficient regulatory mechanisms to quickly acclimate to environmental changes. The most important organs in this process are the nine pairs of gills that not only allow for osmoregulation, but have been shown to be involved in ammonia excretion and respiratory gas exchange. To date, however, little is known about the gills’ contribution to acid-base regulation that might become increasingly important in a “future ocean scenario” whereby surface ocean pH is predicted to drop by up to 0.5 units by the year 2100.
The present thesis aims to characterize the green crab gills’ role in acid-base regulation and how it is linked to ammonia excretion. After exposure to hypercapnia (0.4 kPa pCO2 for 7 days), osmoregulating green crabs were capable of fully compensating for the resulting extracellular respiratory acidosis, while osmoconforming green crabs only partially buffered the accompanying drop in hemolymph pH after acclimation to 1% CO2 for 48 hours. Perfusion experiments on isolated green crab gills showed that different gills contributed to the excretion of H+ in an individual pattern and indicated that NH4+ is an important component of branchial acid excretion. Experiments on gill mRNA expression and pharmaceutical effects on isolated gills identified distinct epithelial transporters to play significant roles in branchial acid base regulation: Rhesus-like protein, basolateral bicarbonate transporter(s), cytoplasmic V-(H+)-ATPase, Na+/H+-exchanger, basolateral Na+/K+-ATPase, cytoplasmic and membrane bound carbonic anhydrase, and basolateral K+ channels. Regarding the latter, the present work provides the first sequence-based evidence for a potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel (CmHCN) capable of promoting NH4+ transport in the green crabs’ gill epithelium, and further demonstrates its direct involvement in branchial acid-base regulation. This highly conserved protein is a potentially important novel key-player in acid-base regulation in all animals.
Interestingly, the observed principles linking acid-base to ammonia regulation in the decapod crustacean gill epithelium resemble many observations previously made in vertebrates. The data of the present thesis therefore provides valuable information for general acid-base regulation, while contributing substantially to our understanding of acid-base regulation in invertebrates.February 2016
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Toshiyuki, Mizota. "The clinical course of anesthetic induction in lung transplant recipients." Kyoto University, 2015. http://hdl.handle.net/2433/202778.
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Kiely, David Gerard. "Cardiopulmonary interactions of hypoxia and hypercapnia and the role of vasoactive mediators in the pulmonary circulation in man." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22375.
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We have examined the cardiopulmonary effects of hypoxia and hypercapnia in the integrated physiological system of normal man using non-invasive pulsed-wave Doppler echocardiography and phonocardiography and have extended this work to study the role vasoactive mediators in the pulmonary circulation in man. We have demonstrated that systolic and diastolic function are unaffected by acute hypercapnia in normal man. Acute hypoxaemia significantly impairs both right and left ventricular diastolic function, in a dose dependent manner, although systolic function remains well preserved. In addition to confirming that hypoxia is a potent pulmonary vasoconstrictor we have demonstrated that hypercapnia is a weak pulmonary vasoconstrictor, suggesting a possible role in ventilation perfusion matching in health and disease. We have also shown potentially adverse electrophysiological effects of both hypoxia and hypercapnia, the clinical significance of which is unknown. The second part of this thesis examines the roles of vasoactive mediators in the pulmonary circulation. In a series of placebo controlled studies we have demonstrated for the first time in normal man that angiotensin II is capable of modulating the acute hypoxic pulmonary vasoconstrictor response, using infusions of the non selective angiotensin II receptor blocker saralasin and the orally active type I angiotensin II receptor blocker losartan. We have extended this work to patients with hypoxaemic cor pulmonale secondary to chronic obstructive pulmonary disease (COPD) and have shown beneficial haemodynamic and endocrine sequelae of type 1 angiotensin II receptor blocking in these patients with a vasoreactive pulmonary circulation. These results suggest that manipulation of the renin-angiotensin system may be of therapeutic benefit in this patient group. We have shown that acute hypoxaemia is a stimulus to endothelin-1 release in normal man and that levels of this peptide are elevated in patients with hypoxaemic cor pulmonale due to COPD.
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Peever, John H. "Day-night differences in ventilation, metabolism, and body temperature during normoxia, hypoxia and hypercapnia in the awake adult rat." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0004/MQ28811.pdf.
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Jones, Myles. "Optical imaging spectroscopy and laser doppler flowmetry in rodent barrel cortex : the hemodynamic response to whisker stimulation and hypercapnia." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251371.
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Checchin, Daniella Marie. "Novel mechanisms for he involvement of hypercapnia in retinal blood flow and neovascularization : implications for retinopathy of prematurity and beyond." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102487.
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Hypercapnia, elevated carbon dioxide (CO2), is an established vasodilator, is present during ischemic episodes, and is a risk factor for retinopathy of prematurity, a disease of the retinal vasculature. Retinopathy of prematurity is an ischemic retinopathy, which like other ischemic pathologies, regresses with the reparation of existing blood vessels and the formation of new ones. However, the potential role of CO2 in this process has been relatively overlooked, particularly in comparison to the numerous studies examining hypoxia in ischemia. Therefore, the central aim of this work was to elucidate how hypercapnia affects the retinal vasculature, impacting blood flow and neovascularization.Retinal blood flow (RBF) studies in hypercapnia-exposed piglets, and rodent models of CO2-induced retinopathy, demonstrate that hypercapnia leads to initial increases in prostaglandin (PG) E2, which mediates an early elevation in RBF, and subsequently augments the endothelial nitric oxide (NO) synthase expression and activity responsible for a later rise in RBF. Ex vivo retinal organ bath experiments and in vitro studies on retinal endothelial cells (ECs) confirmed these findings and revealed that PGE2 increases via EC calcium entry triggered by hypercapnia's accompanying acidosis. While the elevation in RBF creates an oxidative stress, which is detrimental in and of itself, the NO exacerbates this by generating a nitrative stress, resulting in diminished neovascularization. The mechanisms implicated in this include: (1) an altered EC/astrocyte interaction vital to vascularization; (2) the downregulation of the angiogenic PGE 2 receptor EP3; and (3) the direct loss of ECs and microglia, the latter of which we unveil for the first time to have a role in blood vessel development.
Collectively the data suggests that CO2, despite typically being considered rather innocuous, can be detrimental in certain circumstances. In the neonatal retina hypercapnia inappropriately augments RBF via a sequence of events, culminating in a free radical-mediated stress that impairs key players required for proper neovascularization. These findings impart several novel avenues for future research as not only do they improve our understanding of developmental, pathological, and therapeutic retinal neovascularization, but they convey a seminal perspective of CO2 creating a framework within which to examine hypercapnia in other tissues.
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Khemiri, Hanan. "Caractérisation des effets périphériques et centraux de l'érythropoïétine sur la sensibilité chimique à l'O2 et au CO2." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5034.
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L'érythropoïétine (EPO) est une cytokine ayant un rôle important dans l'homéostasie de l'oxygène (O2). Lors d'une hypoxie chronique, l'EPO stimule la maturation des progéniteurs érythroïdes en globules rouges augmentant ainsi le transport de l'O2 aux tissus. Outre cet effet érythropoïétique, l'EPO module la réponse ventilatoire à l'hypoxie (RVH) par une action directe sur la commande centrale respiratoire (CCR) et les chémorécepteurs périphériques. Cet effet a été principalement caractérisé chez des souris mutantes surexprimant l'EPO. Cependant, plusieurs aspects de l'effet de l'EPO sur l'activité du réseau respiratoire demeurent inconnus. Nos résultats montrent qu'une application aigüe d'EPO diminue la dépression centrale hypoxique mesurée in vitro chez le nouveau-né. En revanche, elle n'affecte pas la RVH mesurée in vivo au cours du développement postnatal mais diminue la fréquence des apnées survenant en hypoxie sévère à 6% d'O2. Aussi, chez la souris adulte, l'administration chronique d'EPO et de C-EPO augmente la sensibilité des chémorécepteurs périphériques à l'O2 et maintient la ventilation durant la phase tardive de la RVH. Enfin, l'EPO diminue la sensibilité ventilatoire à l'hypercapnie grâce à des effets périphériques et centraux. L'ensemble de nos résultats montrent que l'EPO module la respiration et contribue à l'homéostasie de l'O2 et du CO2 grâce à ses effets plasmatiques et centraux. Elle représente un candidat à fort potentiel thérapeutique pour les pathologies respiratoires où la sensibilité chimique à l'O2 et au CO2 sont altérés telles que l'apnée du nouveau-né ou le mal chronique des montagnesErythropoietin (EPO) is a cytokine that plays a major role in O2 homeostasis. Upon chronic hypoxia, EPO stimulates the maturation of erythroid progenitors into red blood cells, contributing to increased O2 carrying to tissues. Besides this well-known erythropoietic effect, EPO also modulates the respiratory response to hypoxia by interacting with the central respiratory network in the brainstem and the peripheral chemoreceptors. This effect was mainly characterized in adult mutant mice that overexpress EPO. Several aspects regarding EPO's effect on breathing regulation remain unknown. Our results show that acute EPO treatment increases the O2 sensitivity of the central respiratory network in newborn mice in vitro. However, EPO does not impact the hypoxic ventilatory response to hypoxia in vivo, but decreases the apneic events during severe hypoxia in mice at postnatal day 7. In WT adults, chronic but not acute EPO and C-EPO treatment increases the O2 sensitivity by stimulating both peripheral chemoreceptor and central respiratory network. Finally, both cerebral and plasmatic EPO blunt the ventilatory response to increased CO2 levels in adult mice. Taken together, these results imply that EPO, by acting on the ventilatory system, plays a key role in the modulation of the chemical sensitivity to O2 and CO2
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Fregosi, Ralph, Stuart Quan, Andrew Jackson, Kris Kaemingk, Wayne Morgan, Jamie Goodwin, Jenny Reeder, Rosaria Cabrera, and Elena Antonio. "Ventilatory drive and the apnea-hypopnea index in six-to-twelve year old children." BioMed Central, 2004. http://hdl.handle.net/10150/610096.
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BACKGROUND:We tested the hypothesis that ventilatory drive in hypoxia and hypercapnia is inversely correlated with the number of hypopneas and obstructive apneas per hour of sleep (obstructive apnea hypopnea index, OAHI) in children.METHODS:Fifty children, 6 to 12 years of age were studied. Participants had an in-home unattended polysomnogram to compute the OAHI. We subsequently estimated ventilatory drive in normoxia, at two levels of isocapnic hypoxia, and at three levels of hyperoxic hypercapnia in each subject. Experiments were done during wakefulness, and the mouth occlusion pressure measured 0.1 seconds after inspiratory onset (P0.1) was measured in all conditions. The slope of the relation between P0.1 and the partial pressure of end-tidal O2 or CO2 (PETO2 and PETCO2) served as the index of hypoxic or hypercapnic ventilatory drive.RESULTS:Hypoxic ventilatory drive correlated inversely with OAHI (r = -0.31, P = 0.041), but the hypercapnic ventilatory drive did not (r = -0.19, P = 0.27). We also found that the resting PETCO2 was significantly and positively correlated with the OAHI, suggesting that high OAHI values were associated with resting CO2 retention.CONCLUSIONS:In awake children the OAHI correlates inversely with the hypoxic ventilatory drive and positively with the resting PETCO2. Whether or not diminished hypoxic drive or resting CO2 retention while awake can explain the severity of sleep-disordered breathing in this population is uncertain, but a reduced hypoxic ventilatory drive and resting CO2 retention are associated with sleep-disordered breathing in 6-12 year old children.
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Rohlicek, Charles Vaclav. "Properties of sympathetic neuron responses to cerebral ischemia and to systemic hypoxia or hypercapnia which suggest mediation by central chemosensitive mechanisms." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75944.
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This thesis concerns the possible existence of central nervous system (CNS) chemosensitive mechanisms influencing sympathetic activity. The thesis is based on observations of sympathetic neuron and cardiovascular responses to CNS ischemia, systemic hypoxia and systemic hypercapnia. Investigation of the pressor response to cerebral ischemia in the cat indicates that it is mediated by superficial regions of the ventral medulla also involved in the pressor response to central hypercapnia. Experiments concerning the sympathetic response to systemic hypoxia in the CNS-intact sino-aortic denervated cat revealed a two-component response of the firing rates of single sympathetic preganglionic neurons (SPN), the mass activity of the cervical sympathetic trunk, and the neurogenic component of hindlink vascular resistance (N-HLVR). The response consisted of: (i) an increase of all three variables during extreme hypoxia, and (ii) a decrease during moderate hypoxia. The hypoxic sympatho-depression resulted from loss of central respiratory input to SPNs as well as of respiration-independent input. The hypoxic sympatho-excitation involved only the latter input. Investigation of the sympathetic response to systemic hypercapnia in the acute C$ sb1$ spinal cat demonstrated a direct relationship between SPN firing rate or N-HLVR and arterial PCO$ sb2$ between normocapnia and severe hypercapnia. N-HLVR also increased in this preparation during systemic hypoxia.
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Wright, Chadwick L. "Carbon dioxide and pH effects on thermoregulatory hypothalamic neurons." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1093011603.
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Thesis (Ph. D.)--Ohio State University, 2004.Title from first page of PDF file. Document formatted into pages; contains xviii, 257 p.; also includes graphics (some col.) Includes bibliographical references (p. 245-257).
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Osborne, Salma (Sally). "Effects of hypothermia on ventilation and ventilatory responses to hypercapnia and hypoxia in the golden-mantled ground squirrel and the wistar rat." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28318.
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In this study I examined the effects of progressive hypothermia on minute ventilation, metabolic rate and the ventilatory responses to hypercapnia and hypoxia in the golden-mantled ground squirrel (Spermoohilus lateral is) and the laboratory rat (Rattus norveqicus). These experiments were designed to test the hypothesis that reductions in minute ventilation with progressive body cooling in this species are independant of seasonal changes associated with hibernation and are the result of and therefore parallel the changes in metabolic rate. Similar experiments were carried on the laboratory rat to test the scope of this hypothesis in a non-hibernating mammalian species. Minute ventilation was measured by pneumotachography and carbon dioxide production was measured as an index of metabolic rate. The "helox-cold" method was used to induce progressive hypothermia from 36 to 27°C body temperature under a constant functional plane of halothane anesthesia chosen to suppress shivering. Progressive hypothermia was studied in the ground squirrels during the non-hibernating season and in the laboratory rat throughout the year.
During normothermia, breathing frequency and metabolic rate were approximatley 60% lower in the golden-mantled ground squirrel compared to the rat. In both species. however, hypothermia resulted in proportional decreases in minute ventilation, breathing frequency and metabolic rate. The inspiratory flow rate, an index of respiratory drive was also reduced with decreasing body temperature and showed a similar linear relationship with the ventilatory requirement of each species at any given body temperature. A gradual decrease in duty cycle was observed in both species which was significant only at lower levels of minute ventilation. Breathing remained rhythmic throughout hypothermia although apneic periods occured between breaths at body temperatures below 31°C. The slopes of the ventilatory responses to hypoxia and hypercapnla in the ground squirrel were decreased in proportion to the decreases in minute ventilation and metabolic rate. Ventilatory sensitivity in the rat, however, was not altered.
These results demonstrate that ventilation and metabolic rate are tightly coupled during hypothermia. In addition both species decrease their minute ventilation to match reduced metabolic demands by decreasing breathing frequency alone. Tidal volume is not altered by decreases in body temperature, presumably to ensure adequate alveolar ventilation. The temperature coefficient (Q₁₀) determined in the present study for the effect of body temperature on minute ventilation and metabolic rate in the golden-mantled ground squirrel is similar to that obtained during hibernation in the same species (McArthur, 1986 and Webb, 1987). Consequently, the exponential equations defining the drop in minute ventilation and metabolic rate during progressive hypothermia in the present study accurately predict the values observed at 7°C body temperature during hibernation. It is therefore concluded that ventilation at reduced body temperatures is regulated independantly of the physiological processes that are unique to hibernation and is simply coupled to the metabolic demand of the ground squirrel.Science, Faculty of
Zoology, Department of
Graduate
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Toneloto, Maria Gabriela Cavicchia 1978. "Válvula de oclusão inspiratória regulável e capnografia volumétrica na fístula broncopleural experimental : particularização terapêutica." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308391.
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Orientadores: Antonio Luis Eiras Falcão, Marcos Mello MoreiraTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A fístula broncopleural (FBP) é uma complicação que cursa com elevada mortalidade hospitalar, potencialmente grave quando associada à ventilação mecânica (VM). Desta forma, o presente estudo teve por objetivo, avaliar a eficácia de um sistema valvular de oclusão inspiratória regulável através da avaliação de parâmetros hemodinâmicos, gasométricos e respiratórios, na indução cirúrgica de FBP experimental sob ventilação mecânica invasiva. Foram estudados seis porcos (25kg) submetidos à entubação endotraqueal (TOT), sob VM e monitorado hemodinamicamente com cateter Swan-Ganz. Entre o TOT e o circuito da VM foi conectado o sensor do capnógrafo. Os dados de gasometria arterial e venosa foram registrados antes do ato cirúrgico, após a indução da FBP com débito superior a 50% do volume inspirado e a cada tratamento com a válvula de oclusão inspiratória regulável (VOIr); esta, em diferentes posições de regulagem de fluxo (cinco posições, portanto, cinco tratamentos). Uma extremidade da válvula foi acoplada ao dreno de tórax, enquanto a outra foi colocada entre o TOT e circuito do respirador mecânico. Estatisticamente (p<0,05), as variáveis que apresentaram significância foram o volume corrente alveolar e o débito da FBP. O presente modelo mostrou-se eficaz em sua proposta, sem prejuízos hemodinâmicos, apesar da não constatação da normalização das gasometrias, bem como a não evidência de piora em relação ao tratamento com selo d'água
Abstract: The bronchopleural fistula (BPF) is a complication that takes to higher hospital mortality, potentially severe when associated with mechanical ventilation (MV). Thus, the purpose of this study evaluating the efficacy of a valve system inspiratory occlusion adjustable through evaluation of hemodynamic parameters, arterial blood gas and respiratory in the surgical induction of experimental BPF mechanically ventilated. Were studied six pigs (25kg) underwent endotracheal intubation (ET) under MV and hemodynamically monitored with Swan-Ganz catheter. Between ET and the circuit was connected to the MV capnography sensor. Data from arterial and venous blood gases were recorded before surgical act, after induction of BPF with debt exceeding 50% of the inspired volume and each treatment with inspiratory occlusion valve regulated this in different positions of flow regulation. One end of the valve was attached to the chest tube, while the other was placed between the ET and the circuit of MV. Statistically (p <0.05), the variables that were significant were the alveolar tidal volume and rate of BPF. This model proved effective in its proposal without cause hemodynamic despite not finding the normalization of blood gases as well as no evidence of worsening compared to treatment with water seal
Doutorado
Fisiopatologia Cirúrgica
Doutora em Ciências
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Spencer, Megan A. "Physiological Variability in Juvenile Nine-Banded Armadillos: Responses to Simulated Burrow Conditions During Development." University of Akron / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=akron1312990977.
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Gwozdzinska, Paulina [Verfasser]. "Hypercapnia impairs ENaC cell surface expression and function by promoting phosphorylation and polyubiquitination of ENaC beta-subunit in alveolar epithelial cells / Paulina Gwozdzinska." Gießen : Universitätsbibliothek, 2018. http://d-nb.info/116353370X/34.
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Kryvenko, Vitalii [Verfasser]. "Hypercapnia decreases Na,K-ATPase plasma membrane abundance by impairing endoplasmic reticulum maturation of its beta-subunit in alveolar epithelial cells / Vitalii Kryvenko." Gießen : Universitätsbibliothek, 2021. http://d-nb.info/1233036378/34.
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Rossato, Vivian Biancardi. "Envolvimento da serotonina no controle respiratório durante o desenvolvimento pós-natal." Universidade Federal de São Carlos, 2017. https://repositorio.ufscar.br/handle/ufscar/8983.
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Outra
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Canadian Institutes of Health Research (CIHR)
Serotonin (5-HT) is a neurotransmitter involved in nervous system development, being an important modulator of respiratory rhythm via activation of diverse receptors on respiratory neurons. Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine act as antidepressants and are generally prescribed in depression therapy, including to pregnant women. This study investigated the effects of prenatal (E15-21) exposure to fluoxetine on the ventilatory and metabolic responses to 7% CO2 (hypercapnia) and 10% O2 (hypoxia) of male and female rats during postnatal development (P0-82). To this end, osmotic pumps were implanted subcutaneously in pregnant female rats at embryonic day (E) 15 and delivered vehicle (VEH) or fluoxetine (SSRI, 10 mg/Kg/day) during 7 days. Respiratory frequency (fR), tidal volume (Vt), ventilation (Ve ), O2 consumption (''VO2 ) and air convection requirements (Ve/VO2 ratio) of pups from these litters were studied. In P0-2 male rats, the SSRI group showed a lower Vt and a higher fR in room air conditions, whereas female rats of SSRI group showed a lower Vt in normocapnia normoxica and a higher hyperventilation induced by hypercapnia. At P6-8, male SSRI animals presented a higher fR during hypoxia together with a decrease in the number of neurons that express 5-HT in the caudal dorsal raphe (RDC). P6-8 females from ISRS group showed an attenuated fR during hypoxia. No differences were observed between male rats in the VEH and ISRS groups at P12-14 although there was an increase in the number of 5-HT neurons in the RD. SSRI females showed an attenuated hypercapnic ventilatory response. At P24-26, male SSRI animals showed a lower VEin room air conditions, a higher ventilatory response to hypercapnia and to hypoxia, together with an increase in the number of 5-HT neurons in the ROB and a higher density of TH expression in the LC area. P24-26 SSRI females displayed a lower Ve/V O2 due to a higher V O2 in room air conditions and a higher hyperventilation induced by hypercapnia. In P76-82 male rats, the SSRI group hypoventilated in room air conditions during both wakefulness and NREM sleep and showed a higher increase in Vt induced by hypoxia during wakefulness. These animals showed a higher number of 5-HT neurons in the ROB, RPA and an increase in the number of neurons that express TH in the A5 and in the LC rostral area. Finally, at P76-82, female SSRI rats showed a higher fR in room air conditions during both wakefulness and NREM sleep, an attenuated hypercapnic ventilatory response due to an attenuation of fR during NREM sleep; and an attenuated hypoxic ventilatory response during wakefulness. Also, these animals showed a decrease in the number of 5-HT neurons in the RD. Taken together, these data indicate that SSRI exposure during the prenatal period alters the development of the brainstem respiratory network and results in long lasting and sex specific changes in breathing pattern and in the ventilatory responses to respiratory challenges demonstrating that central and/or peripheric chemoreception may be disrupted in these animals.
A serotonina (5-HT) é um neurotransmissor envolvido no desenvolvimento de vários sistemas neuronais, sendo um importante modulador da ritmogênese respiratória via ativação em diversos receptores nos neurônios respiratórios. Os inibidores seletivos de recaptação de serotonina (ISRSs), como a fluoxetina, agem como antidepressivos e geralmente são prescritos na terapia da depressão, incluindo às mulheres grávidas. Este estudo investigou os efeitos de uma exposição prenatal [dia embrionário (E) 15-21] à fluoxetina nas respostas ventilatórias e metabólicas à hipercapnia (7% CO2) e hipóxia (10% O2) em ratos e ratas durante o desenvolvimento pós-natal (P0-82). Para isso, bombas osmóticas foram implantadas subcutaneamente em ratas grávidas em E15 e forneceram veículo (CTRL) ou fluoxetina (ISRS, 10 mg/Kg/dia) durante 7 dias. A frequência respiratória (fR), o volume corrente (Vt), a ventilação (V e ), o consumo de O2 (V O2) e o equivalente respiratório (V E/VO2) dessas ninhadas foram analisados. Em ratos P0-2, o grupo ISRS apresentou um Vt menor e uma fR maior em ar ambiente. Já as fêmeas do grupo ISRS apresentaram um Vt menor em normocapnia normóxica e um aumento da hiperventilação induzida por hipercapnia. Na idade P6-8, machos ISRS apresentaram uma fR maior durante a hipóxia juntamente com uma queda de 37,9% no número de neurônios que expressam 5-HT na rafe dorsal caudal (RDC), as fêmeas ISRS por sua vez, apresentaram uma fR atenuada em hipóxia em 6%. Nenhuma diferença das varíaveis respiratórias entre grupos foi observada em machos da idade P12-14, porém houve um aumento de 84,7% no número de neurônios que expressam 5-HT na rafe dorsal (RD). As ratas ISRS P12-14 apresentaram uma resposta ventilatória atenuada à hipercapnia. Na idade P24-26, os ratos ISRS demonstraram uma Ve menor em ar ambiente, uma maior resposta ventilatória à hipercapnia e à hipóxia, juntamente com um aumento de 56% no número de neurônios que expressam 5-HT na rafe obscurus (ROB) e uma maior densidade na expressão de tirosina hidroxilase (TH) na região do Locus coeruleus (LC) (16% de aumento). As fêmeas ISRS exibiram um menor V e/V O2 devido a um maior V O2 em normocapnia normóxica e uma maior hiperventilaçao induzida por hipercapnia. Nos ratos P76-82, o grupo ISRS hipoventilou em condições de ar ambiente durante vigília e sono NREM e apresentou um maior aumento no Vt induzido por hipóxia durante a vigília. Estes animais apresentaram um maior número de neurônios que expressam 5-HT na ROB, RPA e um aumento do número de neurônios que expressam TH na região A5 e na região rostral do LC. Finalmente, as fêmeas ISRS da idade P76-82 apresentaram uma maior fR em condições de ar ambiente durante a vigília e o sono NREM, uma resposta ventilatória a hipercapnia atenuada em devido a atenuação da fR durante o sono NREM; e uma resposta ventilatória a hipóxia atenuada durante a vigília. Adicionalmente, estes animais apresentaram uma redução do número de neurônios que expressam 5-HT na RD. Estes resultados, em conjunto, sugerem que uma exposição a ISRS durante o período prenatal altera o desenvolvimento da rede respiratória do tronco encefálico e promove efeitos em longo prazo e sexo específicos na respiração basal como em condições de desafios respiratórios, demonstrando que a quimiorrecepção central e/ou periférica pode estar alterada nestes animais.
CNPq: 209935/2013-8
CNPq: 141653/2012-4
FAPESP: 2012/15298-2
FAPESP: 2012/19966-0
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Matott, Michael Patrick. "The Effects of Oxygen on the Electrophysiology of CO2/H+-Chemosensitive and -Insensitive Neurons of the Solitary Complex of the Rat." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4148.
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This study tested the hypothesis that decreasing the control O2 level from 95% to 40% (5% CO2 + 55% N2) maintains viability in caudal solitary complex (cSC) neurons in transverse slices (~300-400ꝳ) prepared from neonatal rat (P2-22) maintained at 32-34°C. The underlying rationale is to reduce exposure to redox and nitrosative stimuli generated during several hours of exposure to 95% O2 that produces a tissue O2 tension throughout the slice which is in excess of 203 kPa (2.0 atmospheres absolute,ATA) oxygen. Whole cell recordings of cSC neurons maintained in 40% O2 exhibited spontaneous firing and had similar membrane potentials (Vm) and input resistances (Rin) as cSC neurons maintained in 95% O2. Neurons maintained in 40% O2, however, had significantly lower intrinsic firing rates than those maintained in 95% O2. 67% of neurons maintained in 40% O2 control were stimulated by hyperoxia, compared to 81% of neurons maintained in 95% O2 that were stimulated by reoxygenation from relative hypoxia. cSC neurons maintained in 40% O2 also exhibited CO2/H+-sensitivity, including CO2/H+-excitation (31%) and CO2H+-inhibition (31%) and most CO2/H+-sensitive neurons were also stimulated by hyperoxia and reoxygenation or inhibited by lower O2. It is also suggested that acute exposure to lower concentrations of O2 may increase the incidence of CO2-inhibited cSC neurons. Anoxia reduced or eliminated all firing in essentially all cSC neurons. Our findings indicate that brainstem slice viability is retained in 40% O2 control and that hyperoxia is a general stimulant of many cSC neurons, including chemosensitive neurons. We therefore recommend that 40% O2 be used for brainstem electrophysiology studies.
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Lodin, Angelica. "Initiation of spleen contraction resulting in natural blood boosting in humans." Doctoral thesis, Mittuniversitetet, Avdelningen för hälsovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-25518.
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The spleen has been shown to contract in apneic situations in humans as well as in other diving mammals, expelling its stored red blood cell content into circulation. This natural blood boosting may increase the circulating hemoglobin concentration (Hb) by up to 10%, which would enhance the oxygen carrying capacity and likely increase performance. However, the triggers of this response in humans have not been fully clarified. Study I was therefore focused on the effect of hypoxia as a trigger of spleen contraction. It was found that 20 min of normobaric hypoxic breathing evoked a substantial reduction in spleen volume showing that hypoxia is an important trigger for spleen contraction. Knowing the role of hypoxia, Study II compared two different hypoxic situations – a 2 min apnea and 20 min normobaric hypoxic breathing – which resulted in the same level of arterial hemoglobin desaturation. Apnea evoked a twice as great spleen volume reduction, implying that variables other than hypoxia were likely involved in triggering spleen contraction. This may be hypercapnia which is present during apnea but not during normobaric hypoxic breathing. Study III therefore investigated the effects of breathing gas mixtures containing different proportions of CO2 prior to maximal apneas. Pre-breathing mixtures with higher percentages of CO2 resulted in greater spleen contraction, thus demonstrating hypercapnia's likely role as a trigger in addition to hypoxia. Study IV explored whether an all-or-nothing threshold stimulus for triggering spleen contraction existed, or if contraction was graded in relation to the magnitude of triggering stimuli. Exercise was therefore performed in an already hypoxic state during normobaria. Rest in hypoxia produced a moderate spleen volume reduction, with an enhanced spleen contraction resulting after hypoxic exercise, with a concomitant increase in Hb. This implies that spleen contraction is a graded response related to the magnitude of the stimuli. This could be beneficial in environments with varying oxygen content or work loads. Study V examined the possibility that spleen contraction is part of the acclimatization to altitude, during an expedition to summit Mt Everest. The long-term high altitude exposure, combined with physical work on the mountain, had no effects on resting spleen volume but resulted in a stronger spleen contraction, when provoked by apnea or exercise. This indicates that acclimatization to altitude may enhance the contractile capacity of the spleen, which may be beneficial for the climber. From these studies I concluded that hypoxia is an important trigger for spleen contraction but that hypercapnia also contributes in apneic situations. The spleen contraction likely provides a graded expulsion of erythrocytes in response to these stimuli, causing a temporary increase in gas storage capacity that may facilitate activities such as freediving and climbing. The storage of erythrocytes during rest serves to reduce blood viscosity, which would also be beneficial for the climber or diver. The human spleen contraction appears to become stronger with acclimatization, with beneficial effects at altitude. Such an upgraded response could be beneficial both in sports and diseases involving hypoxia.
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Richardson, Matt X. "Hematological changes arising from spleen contraction during apnea and altitude in humans." Doctoral thesis, Mittuniversitetet, Institutionen för naturvetenskap, teknik och matematik, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-7786.
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Bierbower, Sonya M. "ENVIRONMENTAL EFFECTS ON BEHAVIOR AND PHYSIOLOGY IN CRAYFISH." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/778.
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Despite dramatic morphological differences between animals from different taxa, several important features in organization and sensory system processing are similar across animals. Because of this similarity, a number of different organisms including mammals, insects, and decapod crustaceans serve as valuable model systems for understanding general principles of environmental effects. This research examines intrinsic and extrinsic factors by behaviorally and physiologically means to identify the impact of environmental conditions on two distinct crayfish species- Procambarus clarkii (surface) and Orconectes australis packardi (cave).
The research identified behavioral and physiological responses in these two morphological and genetically distinct species. The studies also examined multiple levels of complexity including social behavior, an autonomic response, chemosensory capabilities and neuronal communication, identified comparative similarities/differences, addressed learning and environmental influences on learning and examined behavioral and cellular responses to high levels of carbon dioxide. I found environmental factors directly influence crayfish behavior of social interactions. Interactions were more aggressive, more intense and more likely to end with a physical confrontation when they took place 'in water' than 'out of water'. The modified social interaction resulted in a altered fighting strategy.
A study on motor task learning was undertaken which showed similar learning trends among these crayfish species despite their reliance on different sensory modalities. I also demonstrated learning was dependent on perceived stress by the organism. Previously trained crayfish inhibited from completing a task showed significant increase in an autonomic stress response.
Studies on the behavioral and physiological responses to CO2 revealed that high [CO2] is a repellent in a concentration dependent manner. The autonomic responses in heart rate and an escape tailflip reflex shows complete cessation with high [CO2]. A mechanistic effect of CO2 is by blocking glutamate receptors at the neuromuscular junction and through inhibition of the motor nerve within the CNS.
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Dourado, Débora de Carvalho. "Dimorfismo sexual da função quimiorreceptora a CO2/pH dos neurônios noradrenérgicos no Locus coeruleus." Universidade Federal de São Carlos, 2014. https://repositorio.ufscar.br/handle/ufscar/1254.
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Previous issue date: 2014-04-10Universidade Federal de Minas Gerais
The Locus coeruleus (LC) has been suggested as a CO2 chemoreceptor site in mammals. Most of the studies involving the role of LC in hypercapnic ventilatory response have been performed in males. Since, ovarian steroids modulate the activity of LC neurons and females have a different respiratory response to CO2 of males, we evaluated the activity of LC noradrenergic neurons during normocapnia and hypercapnia in diestrus, ovariectomized (OVX; 0,2 mL/rat of corn oil, s.c., for 3 days) and estradiol-treated ovariectomized (OVX+E2; 10 μg/0,2 mL/rat, s.c., for 3 days) female rats and in intact, orchidectomized (ORX; 0,2 mL/rat of corn oil, s.c., for 7 days), testosterone-treated orchidectomized (ORX+T; 0,25 mg/0,2 mL/rat, s.c., for 7 days) and estradiol-treated orchidectomized (ORX+E2; 10 μg/0,2 mL/rat, s.c., for 3 days) male rats by using double-label immunohistochemistry to c-Fos/TH. Additionally, we assessed the role of noradrenergic LC neurons in OVX and OVX+E2 females on respiratory response to hypercapnia by using 6-hydroxydopamine. Hypercapnia (7% CO2) increased the double-staining (c-Fos/TH-ir) in LC neurons in all groups when compared to air exposure. In the OVX+E2 group there was attenuation in the c-Fos expression in normocapnia and hypercapnia. Hypercapnia increased ventilation in OVX and OVX+E2 groups, which resulted from increases of respiratory frequency (fR) and tidal volume (VT) in sham and 6-OHDA-lesioned groups. The hypercapnic ventilatory response was significantly decreased in 6-OHDA-lesioned rats compared with sham group (29.4% in OVX group and 28.7% in OVX+E2 group) due to a reduced VT in OVX+E2 group and in OVX group due to a decrease in VT and fR. A reduction in TH+ neurons (~61% in OVX and OVX+E2 group) was observed seven days after the microinjections of 6-OHDA in the LC. LC chemical lesion and estradiol did not affect body temperature (Tb). However, hypercapnia caused reduction in Tb of sham (OVX 10 and OVX+E2) and lesioned groups. Thus, we can conclude that noradrenergic neurons in the LC of female and male rats are activated by CO2. However, in OVX+E2 group, estradiol reduced the immunoreactivity compared to OVX group during normocapnia and hypercapnia. Additionally, LC noradrenergic neurons play role in hypercapnic ventilatory response in females but do not affect temperature regulation during normocapnic and hypercapnic conditions.
O Locus coeruleus (LC) é uma área quimiossensível ao CO2 em mamíferos. A maioria dos estudos envolvendo a participação do LC na resposta ventilatória a hipercapnia é realizada em machos. Visto que esteróides ovarianos modulam a atividade de neurônios do LC e fêmeas apresentam uma resposta respiratória ao CO2 diferente de machos, nós avaliamos a atividade dos neurônios noradrenérgicos do LC durante normocapnia e hipercapnia em ratas ciclando em diestro, ovariectomizadas (OVX; 0,2 mL/rata de óleo de milho, s.c., por 3 dias) e ovariectomizadas tratadas com estradiol (OVX+E2; 10 μg/0,2 mL/rata, s.c., por 3 dias) e em ratos intactos, orquidectomizados (ORX; 0,2 mL/rato de óleo de milho, s.c., por 7 dias), orquidectomizados tratados com testosterona (ORX+T; 0,25 mg/0,2 mL/rato, s.c., por 7 dias) e tratados com estradiol (ORX+E2; 10 μg/0,2 mL/rato, s.c., por 3 dias) usando dupla-marcação imunoistoquímica para c-Fos/TH. Adicionalmente, nós avaliamos a participação dos neurônios noradrenérgicos do LC em fêmeas OVX e OVX+E2 na resposta respiratória a hipercapnia usando a neurotoxina 6-hidroxidopamina. A hipercapnia (7% CO2) aumentou a dupla marcação (c-Fos/TH-ir) nos neurônios do LC em todos os grupos comparados a normocapnia. No grupo OVX+E2 houve uma atenuação da expressão de c-Fos no LC em normocapnia e hipercapnia. A hipercapnia causou aumento na ventilação nos grupos OVX e OVX+E2, o qual resultou do aumento da frequência respiratória (fR) e volume corrente (VT) nos grupos controle e lesados. A resposta ventilatória a hipercapnia foi significativamente atenuada no grupo lesado comparado ao grupo controle (29,4% no grupo OVX e 28,7% no grupo OVX+E2) devido à queda no VT no grupo OVX+E2 e no grupo OVX foi devido a queda no VT e na fR. Observamos uma redução de neurônios noradrenérgicos (~61% nos grupos OVX e OVX+E2) sete dias após microinjeções de 6-OHDA no LC. A lesão química do LC e o 8 estradiol não afetaram a Tc. Entretanto, a hipercapnia promoveu redução na temperatura dos grupos sham (OVX e OVX+E2) e lesado. Assim, nós podemos concluir que os neurônios noradrenérgicos do LC de fêmeas e machos são ativados por CO2. Entretanto, no grupo OVX+E2, o estradiol reduziu a imunorreatividade comparado ao grupo OVX durante normocapnia e hipercapnia. Adicionalmente, os neurônios noradrenérgicos do LC de fêmeas participam da resposta ventilatória a hipercapnia, mas não participam da regulação da temperatura durante condições normocápnicas e hipercápnicas.
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Patrone, Luis Gustavo Alexandre. "Participação dos neurônios catecolaminérgicos do tronco encefálico no controle respiratório." Universidade Federal de São Carlos, 2015. https://repositorio.ufscar.br/handle/ufscar/7208.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
It is well know that the respiratory network, undergoes significant development in the postnatal period. Among various processes, the maturing of the catecholaminergic (CA) system shows to be an important factor in the control and modulation of respiratory rhythmogenesis. Studies have also shown that these neurons are widely distributed in the Central Nervous System (CNS), including the A1/C1, A2/C2, C3, A5, A6 and A7 regions, having numerous projections to many regions of the brain. However, the development of respiratory network as well as its effect on the control of ventilation, is not yet fully understood. Thus, understanding the participation of CA neurons in the respiratory control during postnatal development is of most importance for a better understanding of some clinical disorders including Rett Syndrome, Sudden Infant Death Syndrome (SIDS) and Central Congenital Hypoventilation Syndrome (CCHS). Therefore, this study aimed to investigate the involvement of CA neurons in the brainstem on respiratory control in normoxic normocapnic, hypercapnic and hypoxic conditions during the postnatal period of male and female neonatal rats, through chemical injury with conjugated saporin anti-dopamine beta-hydroxylase (DBH-SAP). Thus, DBH-SAP (42 ng/100 nL – 1L), saporin (SAP – 1L) or phosphate buffered solution vehicle (PBS, 0.01M, pH 7.4 – 1L) were injected into the 4th ventricle in male and female neonates Wistar rats P0-1. Pulmonary ventilation ( EV ) was recorded in unanesthetized neonates (P7-8) by pressure plethysmography during normocapnia, hypercapnia (7% CO2) and hypoxia (10% O2) at 10 and 20 min after the start of exposure. Our data demonstrate that lesion of brainstem CA neurons increased ventilation in males and females newborn under room air conditions. In addition, the ventilatory response to hypercapnia was significantly reduced in male (57%) and female (55%) lesioned neonatal rats (Male – SAP group: 212.8 ± 7.0; PBS group: 203.9 ± 10.3; lesioned group: 151.1 ± 7.4; P < 0,001; Female – SAP group: 218.2 ± 10.4; PBS group: 200.0 ± 6.4; lesioned group: 154.0 ± 9.6; P < 0,001; all values relative to % of baseline). Also, a similar reduction was observed in the hypoxic condition (Male – SAP group: 185.2 ± 15.3; PBS group: 167.4 ± 5.0; lesioned group: 110.8 ± 9.2; P < 0,001; Female – SAP group: 197.3 ± 11.8; PBS group: 179.5 ± 13.7; lesioned: 129.4 ± 5.9; P < 0,001; all values relative to % of baseline). Additionally, the values for metabolic rate of control and lesioned groups, both males and females, did not differ significantly, whether in normoxic normocapnic, hypercapnic or hypoxic conditions. These results suggest that brainstem CA neurons exert a tonic inhibitory role in neonatal ventilation and promote an important excitatory modulation in CO2 and O2 chemosensitivity in unanesthetized males and females neonatal rats (P7-8).
Sabe-se que o sistema respiratório, bem como suas vias de controle, sofrem significativo desenvolvimento no período pós-natal. Dentre vários processos, o amadurecimento do sistema catecolaminérgico (CA) mostra-se como um importante fator no controle e modulação da ritmogênese respiratória. Estudos demonstram que esses neurônios estão amplamente distribuídos pelo Sistema Nervo Central (SNC), incluindo as regiões A1/C1, A2/C2, C3, A5, A6 e A7, e que apresentam inúmeras projeções para várias regiões do encéfalo. No entanto, a participação dos neurônios CA no controle respiratório durante o desenvolvimento pós-natal não está bem esclarecido, e esse entendimento é de extrema importância para uma melhor compreensão de alguns problemas clínicos que inclui a Síndrome de Rett, Síndrome da Morte Súbita Infantil (SIDS) e a Síndrome da Hipoventilação Central Congênita (CCHS). Sendo assim, o presente estudo teve por objetivo investigar a participação dos neurônios CA do tronco encefálico no controle respiratório em situações normóxica normocápnicas, hipercápnicas e hipóxicas durante o período pós-natal de ratas e ratos (P7-8), por meio de lesão química com saporina conjugada com anti-dopamina beta-hidroxilase (DBHSAP). Assim, DBH-SAP (42 ng/100 nL – 1L), Saporina (SAP – 1 L) ou veículo solução fosfato tamponado (PBS 0,01 M, pH 7,4 – 1 L) foram injetados no 4° ventrículo de ratas e ratos neonatos Wistar P0-1. A ventilação pulmonar ( EV ) foi registrada em neonatos não anestesiados (P7-8) por pletismografia de pressão, durante normóxia normocápnica, hipercapnia (7% CO2) e hipóxia (10% O2) aos 10 e 20 min após o início da exposição. Nossos dados demonstram que a lesão dos neurônios catecolaminérgicos do tronco encefálico promove um aumento da ventilação em neonatos machos e fêmeas durante a normóxia normocápnica. A resposta ventilatória à hipercapnia foi significativamente reduzida em ratos neonatos lesados (57%) e ratas (55%) (Machos – grupo SAP: 212,8 ± 7,0; grupo PBS: 203,9 ± 10,3; grupo lesado: 151,1 ± 7,4; P < 0,001; Fêmeas – grupo SAP: 218,2 ± 10,4; grupo PBS: 200,0 ± 6,4; grupo lesado: 154,0 ± 9,6; P < 0,001; todos os valores relativos à % do basal). Uma redução similar foi observada na resposta ventilatória à hipóxia (Machos – grupo SAP: 185,2 ± 15,3; grupo PBS: 167,4 ± 5,0; grupo lesado: 110,8 ± 9,2; P < 0,001; Fêmeas – grupo SAP: 197,3 ± 11,8; grupo PBS: 179,5 ± 13,7; grupo lesado: 129,4 ± 5,9; P < 0,001; todos os valores relativos à % do basal). Adicionalmente, os valores referentes às taxas metabólicas de neonatos machos e fêmeas lesados e controles não diferiram significativamente, seja em condição de normóxia normocápnica, hipercapnia ou hipóxia. Esses resultados sugerem que os neurônios catecolaminérgicos localizados no tronco encefálico exercem um papel inibitório tônico sobre ventilação em neonatos P7-8 e apresentam uma importante modulação excitatória na resposta ventilatória ao CO2 e hipóxia em ratas e ratos neonatos (P7-8) não anestesiados.
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Höstman, Staffan. "Minimal volume ventilation in lung injury : With special reference to apnea and buffer treatment." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-305369.
Full textAbstract:
A fairly large portion of patients receiving surgical or intensive care will need mechanical ventilation at some point. The potential ventilator-induced lung injury (VILI) is thus of interest. One of the main causal factors in VILI is the cyclic energy shifts, i.e. tidal volumes, in the lung during mechanical ventilation. The problem can be approached in two ways. Firstly, one can utilize apneic oxygenation and thus not cause any tidal injuries at all. Secondly, and more traditionally, one can simply lower the tidal volumes and respiratory rates used. The following describes a series of animal experiments exploring these options. In the first two papers, I explored and improved upon the methodology of apneic oxygenation. There is a generally held belief that it is only possible to perform apneic oxygenation by prior denitrogenation and by using 100% oxygen during the apnea. As 100% oxygen is toxic, this has prevented apneic oxygenation from more widespread use. The first paper proves that it is indeed possible to perform apneic oxygenation with less than 100% oxygen. I also calculated the alveolar nitrogen concentration which would conversely give the alveolar oxygen concentration. The second paper addresses the second large limitation of apneic oxygenation, i.e. hypercapnia. Using a high dose infusion of tris(hydroxymethyl)aminomethane (THAM) buffer, a pH > 7.2 could be maintained during apneic oxygenation for more than 4.5 hours. In the last two papers, THAM’s properties as a proton acceptor are explored during respiratory acidosis caused by very low volume ventilation. In paper III, I found that THAM does not, in the long term, affect pH in respiratory acidosis after stopping the THAM infusion. It does, however, lower PVR, even though the PaCO2 of THAM-treated animals had rebounded to levels higher than that of the controls. In the last experiment, I used volumetric capnography to confirm our hypothesis that carbon dioxide elimination through the lungs was lower during the THAM infusion. Again, the PaCO2 rebounded after the THAM infusion had stopped and I concluded that renal elimination of protonated THAM was not sufficient.