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Добірка наукової літератури з теми "Hypoxia"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 2 листопада 2024

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Статті в журналах з теми "Hypoxia"

1

Khaytsev, Nikolay Valentinovich, Andrey Glebovich Vasilyev, and Aleksandr Petrovich Trashkov. "THE EFFECT OF ADVANCE HYPOXIC TRAINING UPON TISSUE OXYGEN TENSION IN THE TUMOR DURING AQUTE HYPOXIA OF DIFFERENT TYPES." Pediatrician (St. Petersburg) 4, no. 1 (January 15, 2013): 74–77. http://dx.doi.org/10.17816/ped4174-77.

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The tumors of rats who had not been acclimated to hypoxia subjected to acute hypoxic hypoxia (altitude chamber) as well as blood hypoxia (carbon monoxide) decreased tissue oxygen tension while histotoxic hypoxia (NaCN) on the contrary increased tissue oxygen tension. The tumor acclimated to hypoxia seems to select compensatory mechanisms mostly associated with increased tissue oxygen tension thus taking advantage of lower extent of tissue oxygen tension when subject to acute hypoxic hypoxia than in femoral muscle. All types of acute hypoxias caused a decrease of tissue oxygen tension in the malignancy.

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2

Resta, T. C., J. M. Resta, and B. R. Walker. "Role of endogenous opioids and serotonin in the hemodynamic response to hemorrhage during hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 5 (November 1, 1995): H1597—H1606. http://dx.doi.org/10.1152/ajpheart.1995.269.5.h1597.

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Previous studies from our laboratory indicate that acute but not chronic hypoxia decreases the hemorrhage volume required to elicit reflex hypotension. Furthermore, chronically hypoxic animals exhibit an elevated hypotensive threshold during both normoxia and hypoxia compared with control animals. Because reports suggest that opioid and serotonergic mechanisms may be involved in mediating the sympathoinhibition that occurs with hemorrhage, we hypothesized that opioid and/or serotonergic systems are stimulated during hemorrhage under conditions of acute hypoxia and suppressed after chronic exposure to hypoxia and are thus responsible for the altered cardiovascular responses to hemorrhage under each condition. Control and chronically hypoxi rats were administered either the opioid receptor antagonist naltrexone (1 mg/kg), the selective 5-hydroxytryptamine receptor subtype 3 (5-HT3) serotonergic receptor antagonist MDL-72222 (0.5 mg/kg), or their respective vehicles intravenously before hemorrhage was initiated during normoxia or hypoxia (FIO2 = 0.12). In control animals, pretreatment with naltrexone increased the hemorrhage was initiated volume required to achieve hypotension in hypoxic but not normoxic conditions. Naltrexone had no effect on hypotensive threshold in chronically hypoxic animals under conditions of either normoxia or hypoxia. In addition, MDL-72222 had no effect on hypotensive threshold in either control or chronically hypoxic animals in either normoxic or hypoxic conditions. We conclude that endogenous opioids may contribute to the reflex hypotension that occurs during hypoxic hemorrhage in control rats, while no such involvement is evident in chronically hypoxic animals. Furthermore, peripheral 5-HT3 receptors are not likely involved in this response during either normoxic or hypoxic hemorrhage in control or chronically hypoxic rats.

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3

Voronina, Tatiana A. "The role of hypoxia in stroke and convulsive states. Antihypoxants." Reviews on Clinical Pharmacology and Drug Therapy 14, no. 1 (March 15, 2016): 63–70. http://dx.doi.org/10.17816/rcf14163-70.

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The review deals with the main types of hypoxia and the reasons leading to its development, discusses the development of mechanisms of hypoxiа. Particular attention is paid to brain hypoxia and its role in the development of strokes and convulsive states. The features of the application of antihypoxants and antioxidants at different hypoxic conditions including stroke and seizures are discussed.

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4

Lowry, T. F., H. V. Forster, M. J. Korducki, A. L. Forster, and M. A. Forster. "Comparison of ventilatory responses to sustained reduction in arterial oxygen tension vs. content in awake ponies." Journal of Applied Physiology 76, no. 5 (May 1, 1994): 2147–53. http://dx.doi.org/10.1152/jappl.1994.76.5.2147.

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To gain insight into central and peripheral contributions to changes in breathing during hypoxia, we compared effects on breathing of reducing inspired PO2 (hypoxic hypoxia) with reducing arterial O2 content (CaO2) through elevation of carboxy-hemoglobin (COHb) (CO hypoxia). Twelve awake ponies were studied during 1 h of breathing room air followed by 6 h when COHb was increased to 25% and CaO2 was decreased by 17%. When COHb was increased, arterial PCO2 (PaCO2) increased gradually to 1.3 Torr above (P < 0.05) control level between 30 and 45 min of CO exposure. Pulmonary ventilation (VE) decreased (P = 0.09) approximately 1 liter the first 30 min of CO exposure. After approximately 45 min, PaCO2 began to decrease, steadily reaching 1.5 Torr below (P < 0.05) control level by 4.5 h of CO hypoxia. VE did not change significantly after 30 min of elevated COHb. Eight ponies were also studied during 5 h of hypoxic hypoxia (arterial PO2 approximately 40 Torr). PaCO2 decreased 5 Torr (P < 0.05) within 5 min of hypoxia and decreased another 4 Torr (P < 0.05) between 30 min and 5 h of hypoxia consistent with hypoxic ventilatory acclimatization. VE increased (P < 0.05) within 3 min of hypoxic hypoxia but then decreased (P < 0.05; VE roll off) toward control and did not increase significantly with acclimatization. Because CO and hypoxic hypoxia both decrease brain oxygenation but only hypoxic hypoxia increases carotid chemoreceptor activity, we conclude that initial hypoventilation with CO hypoxia and VE roll off with hypoxic hypoxia are consistent with hypoxic ventilatory depression within the brain. In addition, hyperventilation with prolonged CO hypoxia is consistent with a central nervous system mechanism contributing to this phase of hypoxic ventilatory acclimatization in ponies.

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5

Conde, S. V., E. C. Monteiro, R. Rigual, A. Obeso, and C. Gonzalez. "Hypoxic intensity: a determinant for the contribution of ATP and adenosine to the genesis of carotid body chemosensory activity." Journal of Applied Physiology 112, no. 12 (June 15, 2012): 2002–10. http://dx.doi.org/10.1152/japplphysiol.01617.2011.

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Excitatory effects of adenosine and ATP on carotid body (CB) chemoreception have been previously described. Our hypothesis is that both ATP and adenosine are the key neurotransmitters responsible for the hypoxic chemotransmission in the CB sensory synapse, their relative contribution depending on the intensity of hypoxic challenge. To test this hypothesis we measured carotid sinus nerve (CSN) activity in response to moderate and intense hypoxic stimuli (7 and 0% O2) in the absence and in the presence of adenosine and ATP receptor antagonists. Additionally, we quantified the release of adenosine and ATP in normoxia (21% O2) and in response to hypoxias of different intensities (10, 5, and 2% O2) to study the release pathways. We found that ZM241385, an A2 antagonist, decreased the CSN discharges evoked by 0 and 7% O2 by 30.8 and 72.5%, respectively. Suramin, a P2X antagonist, decreased the CSN discharges evoked by 0 and 7% O2 by 64.3 and 17.1%, respectively. Simultaneous application of both antagonists strongly inhibited CSN discharges elicited by both hypoxic intensities. ATP release by CB increased in parallel to hypoxia intensity while adenosine release increased preferably in response to mild hypoxia. We have also found that the lower the O2 levels are, the higher is the percentage of adenosine produced from extracellular catabolism of ATP. Our results demonstrate that ATP and adenosine are key neurotransmitters involved in hypoxic CB chemotransduction, with a more relevant contribution of adenosine during mild hypoxia, while vesicular ATP release constitutes the preferential origin of extracellular adenosine in high-intensity hypoxia.

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6

Yang, B. C., and J. L. Mehta. "Alterations in pulmonary artery tone during repeated episodes of hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (September 1, 1995): L293—L298. http://dx.doi.org/10.1152/ajplung.1995.269.3.l293.

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To examine the basis of pulmonary constriction during chronic hypoxia, rat pulmonary artery rings were precontracted and exposed to multiple episodes of hypoxia. The first hypoxic episode resulted in a transient contraction, followed by potent relaxation, and then a slow sustained contraction. Repeated hypoxic exposure resulted in stronger initial contraction and attenuated relaxation. Prolongation of the normoxic interval between hypoxic episodes reversed the attenuation of hypoxic relaxation. Pulmonary artery rings that were deendothelialized or treated with the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester or oxyhemoglobin displayed only hypoxic relaxation without initial or late contractions and no attenuation of relaxation during repeated hypoxia. Pretreatment of rings with indomethacin or adenosine or endothelin receptor antagonists had no effect on the hypoxia-mediated alterations. Thus repetitive exposure to hypoxia results in an increase in initial contraction and a decrease in relaxation of pulmonary artery rings. Frequency of hypoxic episodes and endothelial integrity determine pulmonary tone during repeated hypoxia. However, cyclooxygenase products, adenosine, or endothelin do not play a role in hypoxia-mediated changes in rat pulmonary artery tone.

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7

Long, W., D. Lobchuk, and N. R. Anthonisen. "Ventilatory responses to CO2 and hypoxia after sustained hypoxia in awake cats." Journal of Applied Physiology 76, no. 6 (June 1, 1994): 2262–66. http://dx.doi.org/10.1152/jappl.1994.76.6.2262.

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In humans and cats the ventilatory response to 30 min of isocapnic hypoxia is biphasic with an initial increase followed by a decrease, termed “hypoxic depression.” In humans, 30 min of hypoxia reduces the initial response to a subsequent hypoxic exposure. These experiments were to determine whether the same occurred in cats. Cats were studied while awake. End-tidal Po2 and Pco2 were measured by sampling tracheal gas, and ventilation was measured plethysmographically. In seven cats we measured ventilatory responses to two 30-min periods of isocapnic hypoxia (end-tidal Po2 = 60–65 Torr) separated by 5 min of room air breathing. The first hypoxic response was biphasic, with ventilation increasing to 149% of control at 5 min and decreasing to 117% of control at 25 min. During the second exposure, ventilation was 119% of control at 5 min and 113% of control at 25 min; 30 min of hypoxia depressed the subsequent hypoxic response. Hypoxic depression outlasted the hypoxia, suggesting that it was mediated by relatively slow neurochemical events. In five cats ventilatory responses to 5% CO2 were measured before and 5 min after 30 min of isocapnic hypoxia and before and after 30 min of room air breathing. Hypoxia did not affect CO2 responses. Thus the neurochemical events that cause hypoxic depression appear not to involve the neurons generating the response to CO2 and may be specific to those involved in the hypoxic response.

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8

Dahan, A., D. Ward, M. van den Elsen, J. Temp, and A. Berkenbosch. "Influence of reduced carotid body drive during sustained hypoxia on hypoxic depression of ventilation in humans." Journal of Applied Physiology 81, no. 2 (August 1, 1996): 565–72. http://dx.doi.org/10.1152/jappl.1996.81.2.565.

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To evaluate whether the intact hypoxic drive from the carotid bodies during sustained hypoxia is required for the generation of hypoxic depression of ventilation (VE), 16 volunteers were exposed to two consecutive periods of isocapnic hypoxia (first period 20 min; second period 5 min; end-tidal PO2 45 Torr) separated by 6 min of normoxia. In study A, saline was given. In study B, 3 micrograms.kg-1.min-1 i.v. dopamine (DA), a carotid body inhibitor, was given during the first hypoxic exposure followed by saline during normoxia and the second hypoxic exposure. In study C, 20 min of normoxia with DA preceded 6 min of normoxia and 5 min of hypoxia without DA. The first peak hypoxic VE (PHV) in study A was approximately 100% above normoxic VE. After 20 min of hypoxia, VE declined to 60% above normoxic VE. The second PHV in study A was only 60% of the first PHV. We relate this delayed recovery from hypoxia to "ongoing" effects of hypoxic depression. During DA infusion, the changes in VE due to sustained hypoxia were insignificant (study B). The second PHV in study B was not different from the PHV after air breathing in studies A and C. This indicates that the recovery from sustained hypoxia with a suppressed carotid body drive was complete within 6 min. Our results show that despite central hypoxia the absence of ventilatory changes during 20 min of isocapnic hypoxia due to intravenous DA prevented the generation of central hypoxic depression and the depression of a subsequent hypoxic response.

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9

Yoon, Donghoon, Prem Ponka, and Josef T. Prchal. "Hypoxia. 5. Hypoxia and hematopoiesis." American Journal of Physiology-Cell Physiology 300, no. 6 (June 2011): C1215—C1222. http://dx.doi.org/10.1152/ajpcell.00044.2011.

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Our understanding of organismal responses to hypoxia has stemmed from studies of erythropoietin regulation by hypoxia that led to the discovery of the master regulator of the hypoxic response, i.e., hypoxia-inducible factor (HIF). This is a transcription factor that is now known to induce the expression of a battery of genes in response to hypoxia. HIF-1 and HIF-2 regulate many genes that are involved in erythropoiesis and iron metabolism, which are essential for tissue oxygen delivery.

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10

Zonneveld, Marijke, Tom Keulers, and Kasper Rouschop. "Extracellular Vesicles as Transmitters of Hypoxia Tolerance in Solid Cancers." Cancers 11, no. 2 (January 29, 2019): 154. http://dx.doi.org/10.3390/cancers11020154.

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Tumour hypoxia is a common feature of solid tumours that contributes to poor prognosis after treatment. This is mainly due to increased resistance of hypoxic cells to radio- and chemotherapy and the association of hypoxic cells with increased metastasis development. It is therefore not surprising that an increased hypoxic tumour fraction is associated with poor patient survival. The extent of hypoxia within a tumour is influenced by the tolerance of individual tumor cells to hypoxia, a feature that differs considerably between tumors. High numbers of hypoxic cells may, therefore, be a direct consequence of enhanced cellular capability inactivation of hypoxia tolerance mechanisms. These include HIF-1α signaling, the unfolded protein response (UPR) and autophagy to prevent hypoxia-induced cell death. Recent evidence shows hypoxia tolerance can be modulated by distant cells that have experienced episodes of hypoxia and is mediated by the systemic release of factors, such as extracellular vesicles (EV). In this review, the evidence for transfer of a hypoxia tolerance phenotype between tumour cells via EV is discussed. In particular, proteins, mRNA and microRNA enriched in EV, derived from hypoxic cells, that impact HIF-1α-, UPR-, angiogenesis- and autophagy signalling cascades are listed.

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Більше джерел

Дисертації з теми "Hypoxia"

1

O'Dell, Adam David. "Hypoxia." Bowling Green State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1490629987974442.

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2

Chacaroun, Samarmar. "Stratégies thérapeutiques par conditionnement hypoxique : modalités pratiques et effets sur la santé cardio-respiratoire et métabolique." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAS020/document.

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L’hypoxie désigne une baisse de la biodisponibilité en oxygène au niveau tissulaire. La combinaison de l’hypoxie intermittente et de l’hypercapnie est identifiée dans le cadre de plusieurs maladies respiratoires comme un élément physiopathologique déterminant. Cependant, des travaux de recherche suggèrent qu’une exposition à l’hypoxie hypo- ou normocapnique à l’éveil peut améliorer la santé cardiovasculaire. La combinaison d’une exposition hypoxique et de l’entraînement à l’effort est utilisée par les athlètes pour améliorer la performance sportive aérobie. Des études pilotes récentes y compris chez le malade chronique indiquent que l’exposition à l’hypoxie modérée au repos ou à l’effort chez le patient est susceptible d’induire des gains significatifs en termes de santé cardiovasculaire, de composition corporelle et de statut métabolique.Nous nous sommes intéressés aux effets cardiorespiratoires et tissulaires de l’exposition hypoxique normobarique chez le sujet sain et chez la personne en surpoids ou obèse présentant un risque ou des anomalies cardio-métaboliques. Nous avons étudié l’efficacité de 2 types de conditionnement au repos consistant en une hypoxie continue ou une hypoxie intermittente et un entraînement à l’effort hypoxique par comparaison à la situation normoxique. Nous avons tout d’abord étudié les effets d’une exposition hypoxique à court terme au repos chez 14 sujets sains. Nous avons ensuite étudié les effets cardiorespiratoires, tissulaires, vasculaires et métaboliques d’un programme de conditionnement hypoxique normobarique à moyen terme au repos chez 35 patients en surpoids ou obèse. Nous avons de plus réalisé chez 24 sujets sains une étude préliminaire afin de vérifier la faisabilité et de caractériser les réponses cardio-respiratoires et l’oxygénation tissulaire au cours d’un exercice aigu à charge constante d’intensité modérée ou intermittent intense en hypoxie comparé à une condition placébo normoxique. La dernière étude a consisté à étudier les conséquences cardiorespiratoires, tissulaires, vasculaires et métaboliques d’un programme d’entraînement à l’effort en hypoxie par rapport au même programme en normoxie chez 23 patients en surpoids ou obèses.L’étude réalisée chez le sujet sain met en évidence l’intérêt à court terme d’un conditionnement hypoxique intermittent au repos sur des variables associées aux risques cardiovasculaires (diminution de la pression artérielle systolique en normoxie et augmentation de la variabilité sinusale) et une modulation de l’hypoxie tissulaire. Nous avons montré chez le sujet sain que l’hypoxie combiné à l’exercice aigu provoque une diminution de l’oxygénation musculaire similaire mais une diminution de l’oxygénation du cortex préfrontal plus importante par comparaison à un effort normoxique à même intensité relative. Ensuite, chez le sujet en surpoids ou obèse, nous avons montré que le conditionnement hypoxique passif chronique induit une diminution de la pression artérielle diastolique de repos en normoxie, une augmentation de la réponse ventilatoire hypoxique et une diminution de la variabilité cardiaque (après conditionnement par hypoxie intermittente seulement) et que le conditionnement hypoxique actif chronique améliore l’aptitude maximale aérobie par rapport à une situation placébo normoxique.Les résultats obtenus montrent la faisabilité de plusieurs conditionnements hypoxiques prometteurs au plan vasculaire y compris chez le sujet en surpoids ou obèse limité à l’exercice musculaire. Le conditionnement hypoxique actif montre également des bénéfices accrus sur l’aptitude aérobie. Ces protocoles de conditionnement doivent être affinés en vue d’optimiser leur efficacité en termes de perte de poids et d’amélioration du risque cardio-vasculaire et métabolique dans des populations présentant une obésité associée à une morbidité cardio-métabolique. Ils représentent également une piste thérapeutique innovante dans d’autres pathologies chroniques
Hypoxia refers to a decrease in the oxygen bioavailability at the tissue level. The combination of intermittent hypoxia and hypercapnia is identified in several respiratory diseases as a critical pathophysiological element. However, research suggests that exposure to hypo- or normocapnic hypoxia can improve cardiovascular health. The combination of hypoxic exposure and exercise training has been used by athletes to improve aerobic exercise performance. Recent pilot studies in patients with chronic diseases indicate that exposure to moderate hypoxia at rest or during exercise is likely to induce significant gains in cardiovascular health, body composition and metabolic status.We investigated the effects of normobaric hypoxic exposure on cardiorespiratory and tissue function in healthy subjects, overweight or obese subjects at risk or with cardio-metabolic abnormalities. We assessed the efficacy of 2 types of passive hypoxic conditioning consisting in sustained hypoxia or intermittent hypoxia and hypoxic exercise training in comparison with normoxic condition. First, we assessed the effects of short-term hypoxic exposure at rest in 14 healthy subjects. Then, we evaluated the cardiovascular and metabolic effects of a 8-week normobaric hypoxic conditioning program at rest (intermittent or sustained hypoxia) in 35 overweight or obese patients, compared to placebo normoxic exposure. Next, we conducted a preliminary study in 24 healthy subjects to assess the acute responses to submaximal constant-load and high intensity interval cycling exercise performed in normoxia and in hypoxia. The last study aimed to compare the effect of an 8-week exercise training program performed either in normoxia or hypoxia on maximal aerobic capacity in overweight or obese subjects.In the healthy subject, we emphasized the rapid benefits of intermittent hypoxic conditioning on cardiovascular function (lower baseline systolic blood pressure and increased heart rate variability) and the modulation of tissue deoxygenation in response to hypoxia. We have also shown in healthy subjects that acute exercise (combined with hypoxia causes a similar decrease in muscle oxygenation but a greater prefrontal cortex deoxygenation compared to normoxic condition. Then, in the overweight or obese subject, we have shown that chronic passive hypoxic conditioning induces a decrease in diastolic blood pressure at rest in normoxia, an increase in the hypoxic ventilatory response and a decrease in heart rate variability after intermittent hypoxic conditioning only. In addition, chronic active (exercise training) hypoxic conditioning improves the maximal aerobic capacity compared to placebo normoxic training.Our results show the feasibility of several hypoxic conditioning strategies and their interesting effects on the vascular function in overweight/obese subjects presenting exercise limitations impeding exercise reconditioning. In addition, active hypoxic conditioning showed a greater effect on physical fitness than normoxic exercise training. These hypoxic conditioning strategies must be further optimized to improve their efficacy regarding weight loss and cardiometabolic morbidity in obese. They also represent promising therapeutic opportunities for other chronic diseases

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3

Liang, Dinghua. "Progress towards hypoxia-activated SN-38: the potential to target hypoxic tumors." Bentham Science, 2015. http://hdl.handle.net/1993/31591.

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Solid tumors are commonly subject to hypoxia. Hypoxic cancer cells have undesirable properties such as a high tendency to metastasize and resistance to chemotherapy and radiotherapy. Hypoxia-inducible factors (HIFs) respond to the changes in oxygen levels, orchestrating the transcription of many proteins that are vital for the survival of hypoxic cancer cells. With their parent drug SN-38 as an inhibitor of both topoisomerase 1 and HIF-1, hypoxia-activated SN-38s may have a dual inhibitory effect on hypoxic tumor cells due to hypoxia-targeting and HIF-1 inhibition. To develop hypoxia-activated prodrugs of SN-38; 2-, 3-, and 4-nitrobenzyl SN-38s have been synthesized with good yields (78%, 67% and 68%, respectively). Topoisomerase 1 inhibitory assay on 2- and 4-nitrobenzyl SN-38s and cell viability assay on 2-, 3- and 4-nitrobenzyl SN-38s have been performed. All three derivatives showed less toxicity on K562 cells, which meets the principle of prodrug design. Cyclic voltammetry results suggest that the reduction potentials of these three derivatives may be not high enough for these compounds to be activated. The manner of reduction of three nitrobenzyl SN-38s is quasi-reversible under the testing condition, not against the proposed mechanism of activation. Two new derivatives of SN-38 have been designed to elevate reduction potential and further reduce toxicity. They are to be synthesized and tested for future work.
October 2016

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4

Peters, Caren Lorraine. "Hypoxia in inflammation." Thesis, University of Bath, 2003. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426151.

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5

Lau, Yue-huen Thomas. "Nuclear transcription factors and hypoxia-inducible genes in chronic liver hypoxia." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31939302.

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6

Lau, Yue-huen Thomas, and 劉汝這. "Nuclear transcription factors and hypoxia-inducible genes in chronic liver hypoxia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31939302.

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7

Fantacci, M. "In vivo distribution of Hypoxia-Inducible Factor-1α and DNA fragmentation in hypoxic tumoral and non-tumoral cells: correlation between chronic hypoxia and apoptosis". Doctoral thesis, Università degli Studi di Milano, 2004. http://hdl.handle.net/2434/154279.

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8

Querido, Jordan S. "Intermittent hypoxia : cardiorespiratory and cerebrovascular consequences to acute hypoxia and submaximal exercise." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/32125.

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Intermittent hypoxia (IH) is broadly defined as repeatedly breathing decreased amounts of oxygen (hypoxia) interspersed with periods of room air breathing (normoxia). In animal, human diseased, and healthy human models, research has shown IH to negatively affect cerebrovascular vessel dilation. We have previously shown poikilocapnic (uncontrolled carbon dioxide (CO₂)) IH to blunt the vasodilatory response of a cerebral vessel during acute hypoxia. The purpose of this study was to measure the ventilatory, cardiovascular and cerebrovascular responses to: I) acute hypoxia and; II) to submaximal exercise following an isocapnic (controlled CO₂) IH protocol. Healthy males (n = 9) with normal pulmonary function underwent 10 consecutive days of isocapnic IH (oxyhaemoglobin saturation (SaO₂) = 80%, 1 hr/day). Ventilatory, cardiovascular, and cerebrovascular (transcranial Doppler) responses to acute isocapnic hypoxia (SaO₂ = 80%, 5 minutes) were measured before (PRE-IH) and after (POST-IH) IH. Also, ventilatory, cardiovascular, and cerebrovascular parameters were measured during a submaximal cycle exercise test (50, 100, 150 watts) PRE-IH and POST-IH. To further investigate cerebrovascular regulation during exercise, 5% CO₂ was added for two minutes of each exercise stage. Over the 10 days of IH, there was a significant increase in minute ventilation (VE) during the IH bouts (p<0.05). IH did not significantly alter the ventilatory, cardiovascular, and cerebrovascular responses to acute hypoxia. However, there was a significant association (r = 0.86, p<0.05) between the change in the mean arterial blood pressure (MAP) and mean middle cerebral arterial blood flow velocity (MCAVm) responses to acute hypoxia. Exercise caused significant increases in VE , MCAVm, and MAP (p<0.05), but there were no differences in measured variables between PRE-IH and POST-IH exercise trials (p>0.05). Similarly, hypercapnia caused significant increases in VE and MCAVm (p<0.05), although the magnitude of the response did not change following IH. Our results suggest that the effect of IH on ventilatory, cardiovascular, and cerebrovascular regulation during acute hypoxia is individualistic, and changes in the MAP response may strongly influence the changes in cerebral blood flow (CBF). Also, our results suggest that IH does not alter ventilatory, cardiovascular, or cerebrovascular regulation during submaximal exercise or responsiveness to hypercapnia.
Education, Faculty of
Kinesiology, School of
Graduate

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9

Smith, Quintina Denine. "From here to hypoxia." College Park, Md. : University of Maryland, 2006. http://hdl.handle.net/1903/3614.

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Thesis (M.F.A.) -- University of Maryland, College Park, 2006.
Thesis research directed by: Dept. of Art. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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10

Holland, Jason P. "Hypoxia-Selective Copper Radiopharmaceuticals." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491536.

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This thesis presents detailed experimental and computational investigations into the chemistry of copper(II) and zinc(II) bis(thiosemicarbazonato) complexes as potential' radiopharmaceutical agents for imaging and therapy. Chapter 1 provides an introduction to the field of molecular imaging in medicine with particular emphasis on the role of positron emission tomography in oncology. Key aspects of tumour physiology are discussed, and the effects of tumour hypoxia on radiotherapy and chemotherapy are considered. A range of hypoxia-selective radiopharmaceuticals are also introduced including a review of the chemistry and biochemistry of copper(II) complexes of bis(thiosemicarbazonato) ligands. Finally, the aims of this thesis are described. Chapter 2 is divided into two sections. The first section provides a general introduction to computational chemistry and density functional theory. The second section describes computational studies on a range of copper(II) bis(thiosemicarbazonato) complexes with the specific aim of understanding the molecular origins of hypoxia-selectivity and facilitating the design of new complexes with greater hypoxia-selectivity. Chapter 3 reports detailed electrochemical, spectroscopic and computational studies aimed at elucidating the mechanism of hypoxia-selectivity of copper(II) bis(thiosemicarbazonato) complexes. Spectroelectrochemistry experiments have been used to characterise several new species. The delicate equilibria between reduction, reoxidation, protonation and ligand dissociation are also considered and a new mechanistic scheme is proposed. Chapter 4 describes the design and optimisation of a new synthetic route which facilitates rapid functionalisation of the copper(II) bis(thiosemicarbazonato) ligands with biologically active molecules. The methodology has been used to synthesise zinc(II) and copper(II) bis(thiosemicarbazonato) complexes functionalised with a diverse range of saccharides. Transmetallation from the zinc(II) analogues using copper(II) salts is described as a fast and efficient route for radiolabelling and copper64 radiolabelled complexes have been prepared and characterised by a range of in vitro and in vivo experiments. Chapter 5 describes the results obtained for several projects designed at increasing the scope of copper-based radiopharmaceuticals. Preliminary synthetic studies towards the development of complexes for imaging Parkinsonian-type diseases and strategies for dual radiolabelling are presented. Chapter 6 gives general conclusions and future prospects for the development of copper-based radiopharmaceuticals. Chapter 7 reports all experimental details.

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Книги з теми "Hypoxia"

1

Roach, Robert C., Peter D. Wagner, and Peter H. Hackett, eds. Hypoxia. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-8997-0.

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Huang, L. Eric, ed. Hypoxia. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7665-2.

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Roach, Robert C., Peter D. Wagner, and Peter H. Hackett, eds. Hypoxia. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4757-3401-0.

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Roach, Robert C., Peter D. Wagner, and Peter H. Hackett, eds. Hypoxia. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4711-2.

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Roach, Robert C., Peter H. Hackett, and Peter D. Wagner, eds. Hypoxia. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4899-7678-9.

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Gilkes, Daniele M., ed. Hypoxia. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3633-6.

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7

service), ScienceDirect (Online, ed. Hypoxia. Amsterdam: Academic Press, 2009.

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8

Rosenthal, Myron, Peter L. Lutz, Thomas J. Sick, and Peter W. Hochachka. Surviving Hypoxia. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9780367813048.

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9

Justic, Dubravko, Kenneth A. Rose, Robert D. Hetland, and Katja Fennel, eds. Modeling Coastal Hypoxia. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54571-4.

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Machulla, Hans-Jürgen, ed. Imaging of Hypoxia. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-017-1828-8.

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Частини книг з теми "Hypoxia"

1

Sainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble, et al. "Hypoxia, Focus Hypoxic Hypoxia." In Encyclopedia of Exercise Medicine in Health and Disease, 431–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_107.

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2

Walley, K. R. "Hypoxic Hypoxia." In Tissue Oxygenation in Acute Medicine, 81–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-58268-4_6.

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Harr, Jeffrey N., Philip F. Stahel, Phillip D. Levy, Antoine Vieillard-Baron, Yang Xue, Muhammad N. Iqbal, Jeffrey Chan, et al. "Hypoxic Hypoxia." In Encyclopedia of Intensive Care Medicine, 1185. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1729.

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Sainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble, et al. "Hypoxia, Focus Hypobaric Hypoxia." In Encyclopedia of Exercise Medicine in Health and Disease, 428–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_98.

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5

Brand, Marc. "Hypoxia." In Common Surgical Diseases, 444–48. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4757-2945-0_101.

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Gibson, Gary E. "Hypoxia." In Cerebral Energy Metabolism and Metabolic Encephalopathy, 43–78. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-1209-3_3.

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Gardner, Lawrence B. "Hypoxia." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2926-2.

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8

Jain, K. K. "Hypoxia." In Textbook of Hyperbaric Medicine, 39–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-47140-2_5.

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9

Fischer, Bernd, Kewal K. Jain, Erwin Braun, and Siegfried Lehrl. "Hypoxia." In Handbook of Hyperbaric Oxygen Therapy, 17–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72990-4_3.

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Moses, Marsha A. "Hypoxia." In Encyclopedia of Systems Biology, 935. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1546.

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Тези доповідей конференцій з теми "Hypoxia"

1

Kritchenkov, I. S., M. Samandar, N. A. Zharskaia, S. A. Silonov, E. E. Galenko, D. O. Karpitskaya, and S. P. Tunik. "Ir(III) complexes – sensors for hypoxia detection." In 2024 International Conference Laser Optics (ICLO), 540. IEEE, 2024. http://dx.doi.org/10.1109/iclo59702.2024.10624100.

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Markov, Nikolay, and Vladimir Filatov. "TECHNOLOGIES OF AUTOMATED NOTIFICATION OF HUMAN HEALTH AND PERFORMANCE RISKS UNDER HYPOXIC HYPOXIA." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9d39e494.70316289.

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The technologies of automated notification of health risks and human performance under hypoxic hypoxia are described, which provide the calculation and presentation in real time of visual and acoustic information about the value of the assessment of the reserve time for maintaining human health and performance under hypoxic hypoxia

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Amorim, Ísis Salviano Soares de, Priscyanne Barreto Siqueira, Mariana Moreno de Sousa Rodrigues, and Andre Luiz Mencalha. "GENOMIC AND CLINICAL DATA ANALYSIS OF APE1 PROTEIN, BREAST CANCER STEM CELL PHENOTYPE, AND HYPOXIC TUMOR MICROENVIRONMENT." In Brazilian Breast Cancer Symposium 2022. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s2004.

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Introduction: Breast cancer (BC) is a heterogeneous disease at cellular and molecular levels. BC tumors present a cellular subpopulation of breast cancer stem cells (BCSCs) linked with tumor initiation and progression, recurrence, and therapeutic failure. The BCSC is preferentially found in hypoxic areas of the tumor, which are common features of BC and are significantly associated with worse prognosis. Although hypoxia activates an aggressive BCSC phenotype, the proteins that perform this molecular crossroad are still unknown. Therefore, finding proteins that performed this crossing would help define new promisors’ clinical strategies. Apurine/Apyrimidine Endonuclease 1 (APE1) protein has emerged as a new therapeutic target in cancer treatment and is overexpressed in more aggressive BC tumors. However, the relationship of APE1 with BCSC considering the hypoxia microenvironment does not exist. Objectives: This study aimed to analyze the genomic/transcriptomic and clinical data of the APE1, BCSC phenotype, and hypoxic tumors. Methods: Genomic/transcription data and clinical attributes were collected and clustered on the Xena UCSC platform from The Cancer Genome Atlas (TCGA) BRCA database. Clinical molecular signatures from BCSC and hypoxia-related genes were used to separate BC patients in high or low expression groups for these genes and they evaluated their clinical data, including survival and APE1 expressions. Results: Patients with high expression of BCSC-related genes exhibited worse prognosis and overexpression of APE1. Additionally, high expression of hypoxia-related genes was also associated with worse prognosis and exhibited high levels of APE1. Patients with high expression of BCSC genes also exhibited high levels of hypoxia-related genes. APE1, BCSC, and hypoxia-related genes were more expressed in BC compared to adjacent normal samples. Conclusion: Data suggest that APE1 is overexpressed in hypoxia and BCSC phenotype, which are associated with worse prognosis for BC.

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Кечерюкова, Тахмина Мажитовна, Анна Александровна Шульга, and Анна Сергеевна Гончарова. "IN VIVO STUDY THE ACTION OF HYPOXIC CONDITIONS ON THE PROLIFERATIVE POTENTIAL OF LIVER CANCER CELLS." In Фундаментальные и прикладные исследования. Актуальные проблемы и достижения: сборник статей XXII всероссийской (национальной) научной конференции (Санкт-Петербург, Октябрь 2023). Crossref, 2023. http://dx.doi.org/10.37539/231004.2023.23.56.004.

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Гипоксия играет важную роль во многих биологических процессах, включая пролиферацию клеток. В этом исследовании были определены уровни экспрессии маркера пролиферации Ki-67 в тканях опухоли печени с гипоксическими условиями и без гипоксии. Hypoxia play critical roles in various biological processes, icluding cell proliferation. This study expression of the proliferation marker Ki-67 was measured in liver tumor tissues with hypoxic conditions and without hypoxia.

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Tanishita, Kazuo, Kazuto Masamoto, Iwao Kanno, and Hirosuke Kobayashi. "Biotransport to the Cerebral Tissues Related to the Vascular Diseases." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192501.

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Brain is a highly oxidative organ and its consumption rate of oxygen accounts for 20 percent of that of the whole body. This large consumption rate must be met by continuous supply of oxygen, because lack of oxygen rapidly causes irreversible damage to central nervous system. Acute hypoxic episodes cause a certain pattern of regional damage. Cerebral cortex (e.g., layers III, V, and VI) is one of the most susceptible regions to hypoxia, and damage to sensorimotor function is particularly severe in humans that survive hypoxic/ischemic episodes. However, little is known about whether oxygen transport in intracortical regions relates to such selective vulnerability to hypoxia.

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Klinnikova, A. A., G. A. Danilova та N. P. Aleksandrova. "The role of neuronal NO synthase in the respiratory effects of TNF-α". У VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-115-118.

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It was shown that an increase level of proinflammatory cytokines has a modulating effect on the reflex control of respiration. The aim of this study was to investigate the involvement of neuronal nitric oxide synthase (nNOS) in the mechanisms of the influence of an increased level of Tumor necrosis factor – α (TNF-α) on the hypoxic ventilatory response. To achieve this goal, experiments were carried out on urethane anesthetized rats with intravenous administration of TNF-α before and after pretreatment with 7-nitroindazole specific nNOS inhibitor. The hypoxic ventilation response was assessed by rebreathing with a hypoxic gas mixture before and after administration of TNF-α. We found that TNF-α decreased the ventilatory response to hypoxia. Pretreatment with nNOS inhibitor reduced respiratory effects of TNF-α. Key words: cytokines, TNF-α, hypoxia, chemoreflex, respiration, ventilation, neuronal nitric oxide synthase.

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Kobs, Ryan W., Nidal E. Muvarak, and Naomi C. Chesler. "Hypoxia-Induced Changes in the Mechanical Properties of the Mouse Pulmonary Artery." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43086.

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Hypobaric hypoxia produces pulmonary hypertension in mice which causes pulmonary vascular remodeling. To study the biomechanics of this process, mice were exposed to hypoxia for 0-(control), 10-, and 15-days. Using a pressurized arteriograph system, mechanical properties of the main pulmonary artery were measured and compared to the biological changes in the vessel wall measured histologically. 10- and 15-day hypoxic vessels were significantly stiffer when compared to 0-day vessels. This stiffness correlated with greater elastin and collagen content in the vessel wall.

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Морякина, Светлана Васильевна, Хадижат Адамовна Гагаева, and Тамила Исаевна Матиева. "EFFECTS OF PHYSICAL STRESS ON VISUAL ACUITY IN THE PLAIN AND MOUNTAIN CONDITIONS." In Сборник избранных статей по материалам научных конференций ГНИИ «Нацразвитие» (Санкт-Петербург, Ноябрь 2021). Crossref, 2021. http://dx.doi.org/10.37539/nov322.2021.81.79.007.

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Научная статья посвящена установлению изменений со стороны зрительных функций у студенток старших курсов очно-заочной формы обучения в условиях гипоксической и динамической гипоксии. В период акклиматизации к гипоксической гипоксии в течение пятнадцати дней наблюдалась волнообразность или двухфазность изменения остроты зрения. Повышение с первого по пятый день и постепенное снижение с десятого по пятнадцатый день. Scientific article is devoted to establishing changes on the part of visual functions in students of senior courses of full-time education in conditions of hypoxic and dynamic hypoxia. During the period of acclimatization to hypoxic hypoxia, waviness or two-phase change in visual acuity was observed for fifteen days. Increase from day one to day five and gradual decrease from day ten to day fifteen.

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Bocharov, M. I. "Temporary cardiointerval organization with varying degrees of acute normobaric hypoxia in a healthy person." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-36-40.

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The influence of acute normobaric hypoxia (ANH) on the male heart chronotropic effects was studied. Thus, a mild degree of ANH (14.5 % O2, 20 min), causing a decrease in blood oxygenation by 6.3 abs. %, accompanied by an initial (by 5 min) decrease in the RR and QT intervals. The average degree of ANH (12.3% O2) leads to a decrease in blood oxygenation by 19.7 abs. %. At the same time, in inverse relationship to the developing hypoxemia, RR and QT significantly decrease. Corrected values (Pc, PQc, QRSc, QTc) increase during the action period of an average degree of hypoxia, indicating an increase in the proportion of atrial contraction time, atrioventricular conduction of excitation and electrical ventricular systole in the total RR duration, which, apparently, provides optimal systolic heart effect. Key words: human, hypoxia, blood oxygenation, cardiointervals.

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Danilova, G. А., A. A. Klinnikova та N. P. Aleksandrova. "The role of prostaglandins in the realization of respiratory effects of TNF-α in case of hypoxia". У VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-86-88.

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At the present time very little is known about interactions between systemic inflammation and control of respiration. The aim of this study was to compare the respiratory effects of the main inflammatory cytokine TNF - α before and after pretreatment with diclofenac, a nonspecific cyclooxygenase (COX) inhibitor. In experiments on anesthetized, tracheostomized rats, pneumotachometry method was used to measure peak airflow and respiratory rate. The ventilatory response to hypoxia was investigated by the rebreathing method. It is shown that an increase in the systemic level of TNF – α causes a significant increase in the minute volume of respiration, tidal volume, the average speed of the inspiratory flow. In contrast the slope of the hypoxic ventilatory response decreased after administration of TNF-α. Diclofenac pretreatment eliminated these respiratory effects of TNF - α. The data indicate that the ability of TNF - α to enhance basal ventilation and to reduce the ventilatory hypoxic response is mediated by the cyclooxygenase pathway. Key words: tumor necrosis factor – α, hypoxia, prostaglandins, peripheral chemoreception, respiration.

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Звіти організацій з теми "Hypoxia"

1

Morgan, Thomas, Elizabeth Combs, Megan Clayton, Todd S. Dart, Joseph Fischer, Robert B. O Connor, Andrew Pilmanis, and Sean P. Scully. The Effects of Hypoxic Hypoxia on Cognitive Performance Decay. Fort Belvoir, VA: Defense Technical Information Center, May 2015. http://dx.doi.org/10.21236/ada621541.

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Negri, Cristina, Shyam Nair, Leslie Ovard, and Henriette Jager. Bioenergy Solutions to Gulf Hypoxia. Office of Scientific and Technical Information (OSTI), June 2018. http://dx.doi.org/10.2172/1475550.

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Wang, Weigang. Hypoxia in Invasion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485743.

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Nielsen, T. B., and J. L. Kidwell. Cell Biology of Hypoxia, 1996. Fort Belvoir, VA: Defense Technical Information Center, September 1996. http://dx.doi.org/10.21236/ada340589.

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Mahoney, Sean J. Hypoxia, Monitoring, and Mitigation System. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada590823.

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Mahoney, Sean J. Hypoxia, Monitoring, and Mitigation System. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada604355.

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Mahoney, S. J. Hypoxia, Monitoring, and Mitigation System. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada623229.

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Hewett, Kate J., Ian P. Curry, Edna Rath, and Stephanie M. Collins. Subtle Cognitive Effects of Moderate Hypoxia. Fort Belvoir, VA: Defense Technical Information Center, August 2009. http://dx.doi.org/10.21236/ada511511.

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Phillips, Jeffrey B., Leslie A. Drummond, F. E. Robinson, and Matthew E. Funke. Hypoxia: Exposure Time Until Significant Performance Effects. Fort Belvoir, VA: Defense Technical Information Center, March 2016. http://dx.doi.org/10.21236/ad1006779.

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Marshall, Lynne. Effect of Hypoxia on Speech Recognition in Noise. Fort Belvoir, VA: Defense Technical Information Center, March 1987. http://dx.doi.org/10.21236/ada193943.

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