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Artykuły w czasopismach na temat „Hypoxia”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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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 (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 ma

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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 (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 expo

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Voronina, Tatiana A. "The role of hypoxia in stroke and convulsive states. Antihypoxants." Reviews on Clinical Pharmacology and Drug Therapy 14, no. 1 (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 (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) de

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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 (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 adenosin

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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 (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 inhibi

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7

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 (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

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8

Zonneveld, Marijke, Tom Keulers, and Kasper Rouschop. "Extracellular Vesicles as Transmitters of Hypoxia Tolerance in Solid Cancers." Cancers 11, no. 2 (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 c

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9

Smith, Zachary M., Erin Krizay, Rui Carlos Sá, et al. "Evidence from high-altitude acclimatization for an integrated cerebrovascular and ventilatory hypercapnic response but different responses to hypoxia." Journal of Applied Physiology 123, no. 6 (2017): 1477–86. http://dx.doi.org/10.1152/japplphysiol.00341.2017.

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Ventilation and cerebral blood flow (CBF) are both sensitive to hypoxia and hypercapnia. To compare chemosensitivity in these two systems, we made simultaneous measurements of ventilatory and cerebrovascular responses to hypoxia and hypercapnia in 35 normal human subjects before and after acclimatization to hypoxia. Ventilation and CBF were measured during stepwise changes in isocapnic hypoxia and iso-oxic hypercapnia. We used MRI to quantify actual cerebral perfusion. Measurements were repeated after 2 days of acclimatization to hypoxia at 3,800 m altitude (partial pressure of inspired O2 = 9

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10

Sattiraju, Anirudh, Sangjo Kang, Valerie Marallano, et al. "TAMI-59. RECIPROCAL IMPACT OF CANCER IMMUNITY AND TUMOR HYPOXIA DURING GLIOBLASTOMA PROGRESSION." Neuro-Oncology 23, Supplement_6 (2021): vi210. http://dx.doi.org/10.1093/neuonc/noab196.841.

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Abstract Tumor hypoxia is linked to poor outcome for glioblastoma (GBM), a highly malignant brain cancer, but the underlying mechanisms and the environmental factors that initiate tumor hypoxia are poorly understood. We tracked tumor hypoxia in GBM in immunocompetent mice with a hypoxia sensitive fluorescent reporter combined with single cell transcriptomics. We found that hypoxic GBM cells are quiescent, immunosuppressive and display a mesenchymal transition, all of which are linked to malignant potency. We also captured in vivo hypoxia gene signature, which is more represented in recurrent G

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11

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 (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) separat

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12

Jones, Nicole M., and Marcelle Bergeron. "Hypoxic Preconditioning Induces Changes in HIF-1 Target Genes in Neonatal Rat Brain." Journal of Cerebral Blood Flow & Metabolism 21, no. 9 (2001): 1105–14. http://dx.doi.org/10.1097/00004647-200109000-00008.

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Hypoxic preconditioning induces tolerance to hypoxic-ischemic injury in neonatal rat brain and is associated with changes in gene expression. Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that is strongly induced by hypoxia or the hypoxia-mimetic compound cobalt chloride (CoCl2). Hypoxia-inducible factor-1 modulates the expression of several target genes including the glycolytic enzymes, glucose transporter-1 (GLUT-1), and erythropoietin. Recently, HIF-1 expression was shown to increase after hypoxic and CoCl2 preconditioning in newborn rat brain. To study the involvement of HIF

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13

Merellano-Navarro, Eugenio, Marta Camacho-Cardenosa, Gabriel Peinado Costa, et al. "Effects of Different Protocols of Moderate-Intensity Intermittent Hypoxic Training on Mental Health and Quality of Life in Brazilian Adults Recovered from COVID-19: The AEROBICOVID Double-Blind Randomized Controlled Study." Healthcare 11, no. 23 (2023): 3076. http://dx.doi.org/10.3390/healthcare11233076.

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The aim of this study was to investigate the effects of different protocols of moderate-intensity intermittent hypoxic training in patients who had recovered from COVID-19 on quality of life (QoL) and mental health. The sample of this clinical trial-controlled double-blind study consisted of 67 participants aged 30–69 years, who were organized randomly according to Normoxia, Hypoxia, Hypoxia Recovery or Control Group. Eight weeks of cycle ergometer training were performed with a frequency of three training sessions per week in normoxic or hypoxic conditions (with or without hypoxic recovery).

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14

Yoon, Donghoon, Prem Ponka, and Josef T. Prchal. "Hypoxia. 5. Hypoxia and hematopoiesis." American Journal of Physiology-Cell Physiology 300, no. 6 (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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15

Korducki, M. J., H. V. Forster, T. F. Lowry, and M. M. Forster. "Effect of hypoxia on metabolic rate in awake ponies." Journal of Applied Physiology 76, no. 6 (1994): 2380–85. http://dx.doi.org/10.1152/jappl.1994.76.6.2380.

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To determine the effect of hypoxia on metabolic rate (VO2) of ponies, on 2 days we studied ponies that were breathing room air for 1 h followed by 5 h of either hypoxic hypoxia (fractional concn of inspired O2 = 0.126) or 5 h of CO hypoxia. Control arterial PO2 was 103 +/- 1.2 Torr, and at 5 min and 5 h of hypoxic hypoxia, arterial PO2 was 53.1 +/- 1.8 and 41.0 +/- 1.8 Torr, respectively. There was a time-dependent hypocapnia and alkalosis during hypoxic hypoxia. During CO hypoxia, carboxyhemoglobin increased to 25% after 30 min and remained constant thereafter. With increased carboxyhemoglobi

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16

Kabakov, Alexander E., and Anna O. Yakimova. "Hypoxia-Induced Cancer Cell Responses Driving Radioresistance of Hypoxic Tumors: Approaches to Targeting and Radiosensitizing." Cancers 13, no. 5 (2021): 1102. http://dx.doi.org/10.3390/cancers13051102.

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Within aggressive malignancies, there usually are the “hypoxic zones”—poorly vascularized regions where tumor cells undergo oxygen deficiency through inadequate blood supply. Besides, hypoxia may arise in tumors as a result of antiangiogenic therapy or transarterial embolization. Adapting to hypoxia, tumor cells acquire a hypoxia-resistant phenotype with the characteristic alterations in signaling, gene expression and metabolism. Both the lack of oxygen by itself and the hypoxia-responsive phenotypic modulations render tumor cells more radioresistant, so that hypoxic tumors are a serious chall

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17

Hoshikawa, Yasushi, Sadafumi Ono, Satoshi Suzuki, et al. "Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia." Journal of Applied Physiology 90, no. 4 (2001): 1299–306. http://dx.doi.org/10.1152/jappl.2001.90.4.1299.

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Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with pulmonary vascular remodeling. Because hypoxia might promote generation of oxidative stress in vivo, we hypothesized that oxidative stress may play a role in the hypoxia-induced cardiopulmonary changes and examined the effect of treatment with the antioxidant N-acetylcysteine (NAC) in rats. NAC reduced hypoxia-induced cardiopulmonary alterations at 3 wk of hypoxia. Lung phosphatidylcholine hydroperoxide (PCOOH) increased at days 1 and 7 of the hypoxic exposure, and NAC attenuated the increase in lun

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18

Kammerer, Tobias, Valentina Faihs, Nikolai Hulde, et al. "Hypoxic-Inflammatory Responses under Acute Hypoxia: In Vitro Experiments and Prospective Observational Expedition Trial." International Journal of Molecular Sciences 21, no. 3 (2020): 1034. http://dx.doi.org/10.3390/ijms21031034.

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Induction of hypoxia-inducible-factor-1α (HIF-1α) pathway and HIF-target genes allow adaptation to hypoxia and are associated with reduced incidence of acute mountain sickness (AMS). Little is known about HIF-pathways in conjunction with inflammation or exercise stimuli under acute hypobaric hypoxia in non-acclimatized individuals. We therefore tested the hypotheses that (1) both hypoxic and inflammatory stimuli induce hypoxic-inflammatory signaling pathways in vitro, (2) similar results are seen in vivo under hypobaric hypoxia, and (3) induction of HIF-dependent genes is associated with AMS i

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Ooi, Henry, Elaine Cadogan, Michèle Sweeney, Katherine Howell, R. G. O'Regan, and Paul McLoughlin. "Chronic hypercapnia inhibits hypoxic pulmonary vascular remodeling." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (2000): H331—H338. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h331.

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Chronic hypercapnia is commonly found in patients with severe hypoxic lung disease and is associated with a greater elevation of pulmonary arterial pressure than that due to hypoxia alone. We hypothesized that hypercapnia worsens hypoxic pulmonary hypertension by augmenting pulmonary vascular remodeling and hypoxic pulmonary vasoconstriction (HPV). Rats were exposed to chronic hypoxia [inspiratory O2 fraction ([Formula: see text]) = 0.10], chronic hypercapnia (inspiratory CO2 fraction = 0.10), hypoxia-hypercapnia ([Formula: see text]= 0.10, inspiratory CO2 fraction = 0.10), or room air. After

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Chen, Chien-Yi, Wei-Zen Sun, Kai-Hsiang Kang, et al. "Hypoxic Preconditioning Suppresses Glial Activation and Neuroinflammation in Neonatal Brain Insults." Mediators of Inflammation 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/632592.

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Perinatal insults and subsequent neuroinflammation are the major mechanisms of neonatal brain injury, but there have been only scarce reports on the associations between hypoxic preconditioning and glial activation. Here we use neonatal hypoxia-ischemia brain injury model in 7-day-old rats andin vitrohypoxia model with primary mixed glial culture and the BV-2 microglial cell line to assess the effects of hypoxia and hypoxic preconditioning on glial activation. Hypoxia-ischemia brain insult induced significant brain weight reduction, profound cell loss, and reactive gliosis in the damaged hemis

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Mouradian, Gary C., Satyan Lakshminrusimha, and Girija G. Konduri. "Perinatal Hypoxemia and Oxygen Sensing." Comprehensive Physiology 11, no. 2 (2021): 1653–77. https://doi.org/10.1002/j.2040-4603.2021.tb00155.x.

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AbstractThe development of the control of breathing begins in utero and continues postnatally. Fetal breathing movements are needed for establishing connectivity between the lungs and central mechanisms controlling breathing. Maturation of the control of breathing, including the increase of hypoxia chemosensitivity, continues postnatally. Insufficient oxygenation, or hypoxia, is a major stressor that can manifest for different reasons in the fetus and neonate. Though the fetus and neonate have different hypoxia sensing mechanisms and respond differently to acute hypoxia, both responses prevent

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Cha, Ryota, Shuji Nakagawa, Yuji Arai та ін. "Intermittent hypoxic stimulation promotes efficient expression of Hypoxia-inducible factor-1α and exerts a chondroprotective effect in an animal osteoarthritis model". PLOS ONE 20, № 4 (2025): e0319976. https://doi.org/10.1371/journal.pone.0319976.

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Hypoxia-inducible factor-1α plays an important role in the homeostasis of articular cartilage in hypoxic environments. Therefore, modulation of hypoxia-inducible factor-1α by regulating the oxygen environment could be a useful treatment for osteoarthritis. This study aimed to assess the chondroprotective effects of intermittent hypoxia on cultured chondrocytes and an animal model of osteoarthritis. In vitro, human chondrocytes were exposed to 2 h of hypoxic stimulation three times at 1-h intervals, and protein and gene expression of hypoxia-inducible factor-1α, ACAN, and cell viability was mea

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Neubert, Elias, Beate Rassler, Annekathrin Hoschke, Coralie Raffort, and Aida Salameh. "Effects of Normobaric Hypoxia and Adrenergic Blockade over 72 h on Cardiac Function in Rats." International Journal of Molecular Sciences 24, no. 14 (2023): 11417. http://dx.doi.org/10.3390/ijms241411417.

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In rats, acute normobaric hypoxia depressed left ventricular (LV) inotropic function. After 24 h of hypoxic exposure, a slight recovery of LV function occurred. We speculated that prolonged hypoxia (72 h) would induce acclimatization and, hence, recovery of LV function. Moreover, we investigated biomarkers of nitrosative stress and apoptosis as possible causes of hypoxic LV depression. To elucidate the role of hypoxic sympathetic activation, we studied whether adrenergic blockade would further deteriorate the general state of the animals and their cardiac function. Ninety-four rats were expose

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Ono, Yoko, and Hidemasa Bono. "Multi-Omic Meta-Analysis of Transcriptomes and the Bibliome Uncovers Novel Hypoxia-Inducible Genes." Biomedicines 9, no. 5 (2021): 582. http://dx.doi.org/10.3390/biomedicines9050582.

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Hypoxia is a condition in which cells, tissues, or organisms are deprived of sufficient oxygen supply. Aerobic organisms have a hypoxic response system, represented by hypoxia-inducible factor 1-α (HIF1A), to adapt to this condition. Due to publication bias, there has been little focus on genes other than well-known signature hypoxia-inducible genes. Therefore, in this study, we performed a meta-analysis to identify novel hypoxia-inducible genes. We searched publicly available transcriptome databases to obtain hypoxia-related experimental data, retrieved the metadata, and manually curated it.

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Pasha, Musayev-Galbinur, Markitantova Yuliya, Babayev Khanagha, and Akberova Sevinj. "Hypoxia-induced apoptosis of eyeball cells." Journal of Life Sciences and Biomedicine 2023, no. 1 (2023): 38–41. https://doi.org/10.5281/zenodo.8004205.

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We aimed to study the effect of acute hypoxic hypoxia and acute hypobaric hypoxia on eye tissue cells in adult rats. In each experiment with acute hypoxic hypoxia and acute hypobaric hypoxia, 12 (4 animals in each group, 24 rats in total) male Wistar rats (24 eyes in each experiment, 48 eyes in total) were used, divided into 3 groups: Group I - intact control, group II - 1 hour after hypoxia, group III - 3 hours after hypoxia. Identification of apoptotic cells in the tissues of the eye was performed by the TUNEL method on frozen eye sections with additional staining with nuclear fluorescent dy

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Micaux, Julia, Abir Troudi Habibi, Franck Mauconduit, and Marion Noulhiane. "Hypoxia’s Impact on Hippocampal Functional Connectivity: Insights from Resting-State fMRI Studies." Brain Sciences 15, no. 6 (2025): 643. https://doi.org/10.3390/brainsci15060643.

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The hippocampus is one of the brain’s most vulnerable structures to hypoxia, playing a crucial role in memory and spatial navigation. This sensitivity makes it a key region for understanding the effects of hypoxia on brain connectivity. This review examines the effects of both acute and chronic hypoxia on resting-state networks (RSNs) that contribute to hippocampal functional connectivity (FC). Hypoxia, characterized by a reduced oxygen supply to the brain, can result from environmental factors (such as high-altitude exposure) or hypoxia-induced pathological conditions (including obstructive s

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Pantazopoulou, Vasiliki, Pauline Jeannot, Rebecca Rosberg, Tracy J. Berg, and Alexander Pietras. "Hypoxia-Induced Reactivity of Tumor-Associated Astrocytes Affects Glioma Cell Properties." Cells 10, no. 3 (2021): 613. http://dx.doi.org/10.3390/cells10030613.

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Glioblastoma is characterized by extensive necrotic areas with surrounding hypoxia. The cancer cell response to hypoxia in these areas is well-described; it involves a metabolic shift and an increase in stem cell-like characteristics. Less is known about the hypoxic response of tumor-associated astrocytes, a major component of the glioma tumor microenvironment. Here, we used primary human astrocytes and a genetically engineered glioma mouse model to investigate the response of this stromal cell type to hypoxia. We found that astrocytes became reactive in response to intermediate and severe hyp

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Yu, Albert C. H., George A. Gregory, and Pak H. Chan. "Hypoxia-Induced Dysfunctions and Injury of Astrocytes in Primary Cell Cultures." Journal of Cerebral Blood Flow & Metabolism 9, no. 1 (1989): 20–28. http://dx.doi.org/10.1038/jcbfm.1989.3.

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The effects of severe hypoxia were studied in a primary culture of astrocytes prepared from newborn rat cerebral cortex. Hypoxia was created by placing cultures in an airtight chamber that was flushed with 95% N2/5% CO2 for 15 min before being sealed. The hypoxic environment was maintained constant for up to 24 h. During the first 12 h of hypoxia, astrocytes showed no morphological changes by phase-contrast microscopy. After 18 h of hypoxia, some astrocytes in culture became swollen and started to detach from the culture dish. All cells in the culture were destroyed after 24 h of hypoxia. The

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Frappell, P. B., and J. P. Mortola. "Hamsters vs. rats: metabolic and ventilatory response to development in chronic hypoxia." Journal of Applied Physiology 77, no. 6 (1994): 2748–52. http://dx.doi.org/10.1152/jappl.1994.77.6.2748.

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The postnatal developments of the rat and hamster were compared after the animals were raised from birth for 21 days either in normoxia (control animals) or chronic hypoxia (PO2 of 80–90 Torr). Compared with control rats, hypoxic rats had a reduction in body mass. Hypoxic rats had lowered O2 consumption (VO2) and increased (67%) ventilation (VE), whereas hypoxic hamsters maintained the same metabolic rate as control hamsters but increased VE by 100%. As a result, when raised in hypoxia both species increased VE/VO2 to the same extent. When acutely exposed to hypoxia, control animals of both sp

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Nieuwenhuijs, Diederik, Elise Sarton, Luc Teppema, and Albert Dahan. "Propofol for Monitored Anesthesia Care." Anesthesiology 92, no. 1 (2000): 46. http://dx.doi.org/10.1097/00000542-200001000-00013.

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Background Hypoxia has a dual effect on ventilation: an initial period of hyperventilation, the acute hypoxic response, is followed after 3-5 min by a slow decline, the hypoxic ventilatory decline. Because of hypoxic ventilatory decline, subsequent acute hypoxic responses are depressed. In this study, the influence of a sedative concentration of propofol on ventilation was studied if hypoxia was sustained and intermittent. Methods Ten healthy young male volunteers performed two hypoxic tests without and with a target controlled infusion of propofol. The sustained hypoxic test consisted of 15 m

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Dyba, Iryna, Ervin Asanov, Seviliya Asanova, and Juliya Holubova. "Hypoxia resistance among the agedpatients with chronic obstructive lung disease: possibilities of using hypoxic trains." Ageing & Longevity 1, no. 1 (2020): 12–18. http://dx.doi.org/10.47855/jal9020-2020-1-3.

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Age-related morphological and functional changes in the body lead to the development of arterial hypoxemia, tissue hypoxia and hypoxic changes, which reduces the body's resistance to hypoxia and contributes to the development of lung diseases, in particular chronic obstructive pulmonary disease (COPD) in the elderly. The aim of the study was to clarify the effect of interval normobaric hypoxic training (INHT) on hypoxia resistance in elderly patients with COPD. The survey showed that with an increase in bronchial obstruction, the shifts of blood saturation during hypoxia increase. The course o

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Halliwill, John R., and Christopher T. Minson. "Cardiovagal regulation during combined hypoxic and orthostatic stress: fainters vs. nonfainters." Journal of Applied Physiology 98, no. 3 (2005): 1050–56. http://dx.doi.org/10.1152/japplphysiol.00871.2004.

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We tested the hypothesis that individual differences in the effect of acute hypoxia on the cardiovagal arterial baroreflex would determine individual susceptibility to hypoxic syncope. In 16 healthy, nonsmoking, normotensive subjects (8 women, 8 men, age 20–33 yr), we assessed orthostatic tolerance with a 20-min 60° head-upright tilt during both normoxia and hypoxia (breathing 12% O2). On a separate occasion, we assessed baroreflex control of heart rate (cardiovagal baroreflex gain) using the modified Oxford technique during both normoxia and hypoxia. When subjects were tilted under hypoxic co

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Yang, Shanshan, Yan Cui, Rui Ma та ін. "Hypoxia Regulates the Proliferation and Apoptosis of Coronary Artery Smooth Muscle Cells Through HIF-1α Mediated Autophagy in Yak". Biomolecules 15, № 2 (2025): 256. https://doi.org/10.3390/biom15020256.

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Cell proliferation and migration mediated by hypoxia-inducible factor-1α (HIF-1α) are important processes of hypoxic cardiac vascular remodeling. HIF-1α also regulates the physiological hypoxic adaptation of the coronary artery in the yak heart, but the potential mechanism remains to be completely elucidated. In this study, coronary artery proliferation increased with age and hypoxia adaptation time. In vitro analysis showed that hypoxia can promote the proliferation of coronary vascular smooth muscle cells (CASMCs). Meanwhile, HIF-1α plays an important role in the regulation of proliferation

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Yang, B. C., and J. L. Mehta. "Critical role of endothelium in sustained arterial contraction during prolonged hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 3 (1995): H1015—H1020. http://dx.doi.org/10.1152/ajpheart.1995.268.3.h1015.

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Acute anoxia or severe hypoxia causes an initial transient contraction followed by marked relaxation of vascular tissues. We observed a spontaneous gradual sustained contraction of rat aortic rings following relaxation when hypoxia was prolonged. Deendothelialization as well as treatment of the endothelium-intact rings with nitric oxide synthase inhibitors or oxyhemoglobin abolished the late hypoxic contraction despite prolonged hypoxia. The prolonged hypoxia-induced sustained contraction was not affected by adenosine receptor blockade, cyclooxygenase inhibition, free radical scavengers, or th

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Martinez, Chloe-Anne, Bernadette Kerr, Charley Jin, Peter Cistulli, and Kristina Cook. "Obstructive Sleep Apnea Activates HIF-1 in a Hypoxia Dose-Dependent Manner in HCT116 Colorectal Carcinoma Cells." International Journal of Molecular Sciences 20, no. 2 (2019): 445. http://dx.doi.org/10.3390/ijms20020445.

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Obstructive sleep apnea (OSA) affects a significant proportion of the population and is linked to increased rates of cancer development and a worse cancer outcome. OSA is characterized by nocturnal intermittent hypoxia and animal models of OSA-like intermittent hypoxia show increased tumor growth and metastasis. Advanced tumors typically have regions of chronic hypoxia, activating the transcription factor, HIF-1, which controls the expression of genes involved in cancer progression. Rapid intermittent hypoxia from OSA has been proposed to increase HIF-1 activity and this may occur in tumors. T

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Airlie, M. A. A., D. C. Flenley, and P. M. Warren. "Effect of Almitrine on Hypoxic Ventilatory Drive Measured by Transient and Progressive Isocapnic Hypoxia in Normal Men." Clinical Science 77, no. 4 (1989): 431–37. http://dx.doi.org/10.1042/cs0770431.

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1. In a double-blind placebo-controlled study, we have investigated the effect of the peripheral chemoreceptor stimulant drug almitrine bismesylate on hypoxic ventilatory drive (expressed as the slope of the minute ventilation/arterial oxygen saturation relationship in litres min−1 %−1) as measured by both progressive isocapnic hypoxia at rest and transient hypoxia (three breaths of 100% N2) during moderate exercise, in seven normal men, to determine if the ventilatory response to the transient hypoxic stimulus is a more specific measure of peripheral chemoreceptor sensitivity to hypoxia. 2. H

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Brendel, Heike, Jennifer Mittag, Anja Hofmann, et al. "NADPH Oxidase 4: Crucial for Endothelial Function under Hypoxia—Complementing Prostacyclin." Antioxidants 13, no. 10 (2024): 1178. http://dx.doi.org/10.3390/antiox13101178.

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Aim: The primary endothelial NADPH oxidase isoform 4 (NOX4) is notably induced during hypoxia, with emerging evidence suggesting its vasoprotective role through H2O2 production. Therefore, we aimed to elucidate NOX4′s significance in endothelial function under hypoxia. Methods: Human vessels, in addition to murine vessels from Nox4-/- mice, were explored. On a functional level, Mulvany myograph experiments were performed. To obtain mechanistical insights, human endothelial cells were cultured under hypoxia with inhibitors of hypoxia-inducible factors. Additionally, endothelial cells were cultu

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Cutler, Michael J., Nicolette Muenter Swift, David M. Keller, Wendy L. Wasmund, and Michael L. Smith. "Hypoxia-mediated prolonged elevation of sympathetic nerve activity after periods of intermittent hypoxic apnea." Journal of Applied Physiology 96, no. 2 (2004): 754–61. http://dx.doi.org/10.1152/japplphysiol.00506.2003.

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Obstructive sleep apnea (OSA) is associated with transient elevation of muscle sympathetic nerve activity (MSNA) during apneic events, which often produces elevated daytime MSNA in OSA patients. Hypoxia is postulated to be the primary stimulus for elevated daytime MSNA in OSA patients. Therefore, we studied the effects of 20 min of intermittent voluntary hypoxic apneas on MSNA during 180 min of recovery. Also, we compared MSNA during recovery after either 20 min of intermittent voluntary hypoxic apneas, hypercapnic hypoxia, or isocapnic hypoxia. Consistent with our hypothesis, both total MSNA

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Wodopia, Ralf, Hyun Soo Ko, Javiera Billian, Rudolf Wiesner, Peter Bärtsch, and Heimo Mairbäurl. "Hypoxia decreases proteins involved in epithelial electrolyte transport in A549 cells and rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 6 (2000): L1110—L1119. http://dx.doi.org/10.1152/ajplung.2000.279.6.l1110.

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Fluid reabsorption from alveolar space is driven by active Na reabsorption via epithelial Na channels (ENaCs) and Na-K-ATPase. Both are inhibited by hypoxia. Here we tested whether hypoxia decreases Na transport by decreasing the number of copies of transporters in alveolar epithelial cells and in lungs of hypoxic rats. Membrane fractions were prepared from A549 cells exposed to hypoxia (3% O2) as well as from whole lung tissue and alveolar type II cells from rats exposed to hypoxia. Transport proteins were measured by Western blot analysis. In A549 cells, α1- and β1-Na-K-ATPase, Na/K/2Cl cotr

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White, Hilary A., Yi Jin, Louis G. Chicoine, Bernadette Chen, Yusen Liu, and Leif D. Nelin. "Hypoxic proliferation requires EGFR-mediated ERK activation in human pulmonary microvascular endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 5 (2017): L649—L656. http://dx.doi.org/10.1152/ajplung.00267.2016.

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We have previously shown that hypoxic proliferation of human pulmonary microvascular endothelial cells (hPMVECs) depends on epidermal growth factor receptor (EGFR) activation. To determine downstream signaling leading to proliferation, we tested the hypothesis that hypoxia-induced proliferation in hPMVECs would require EGFR-mediated activation of extracellular signal-regulated kinase (ERK) leading to arginase II induction. To test this hypothesis, hPMVECs were incubated in either normoxia (21% O2, 5% CO2) or hypoxia (1% O2, 5% CO2) and Western blotting was performed for EGFR, arginase II, phos

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Ogata, M., M. Ohe, D. Katayose, and T. Takishima. "Modulatory role of EDRF in hypoxic contraction of isolated porcine pulmonary arteries." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 3 (1992): H691—H697. http://dx.doi.org/10.1152/ajpheart.1992.262.3.h691.

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To examine the hypothesis that suppression of basal release of endothelium-derived relaxing factor (EDRF) by hypoxia might be related to the mechanism of hypoxic pulmonary vasoconstriction, rings of porcine pulmonary artery (PA, 2 mm OD) were suspended in organ chambers and changes in isometric force were measured. Hypoxia significantly reduced endothelium-dependent relaxation induced by acetylcholine and augmented contractile response to phenylephrine. This augmentation by hypoxia was not seen in rings without endothelium. Contractile response to phenylephrine was also enhanced by removal of

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Huynh, Kenneth N., Sriram Rao, Bradley Roth та ін. "Targeting Hypoxia-Inducible Factor-1α for the Management of Hepatocellular Carcinoma". Cancers 15, № 10 (2023): 2738. http://dx.doi.org/10.3390/cancers15102738.

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Hypoxia-inducible factor 1 alpha (HIF-1α) is a transcription factor that regulates the cellular response to hypoxia and is upregulated in all types of solid tumor, leading to tumor angiogenesis, growth, and resistance to therapy. Hepatocellular carcinoma (HCC) is a highly vascular tumor, as well as a hypoxic tumor, due to the liver being a relatively hypoxic environment compared to other organs. Trans-arterial chemoembolization (TACE) and trans-arterial embolization (TAE) are locoregional therapies that are part of the treatment guidelines for HCC but can also exacerbate hypoxia in tumors, as

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Dzhalilova, D. Sh, A. M. Kosyreva, I. S. Tsvetkov, and O. V. Makarova. "Phagocytic activity of peripheral blood monocytes under <i>in vivo</i> and <i>in vitro</i> hypoxia conditions in tolerant and susceptible to oxygen deficiency rats." Medical Immunology (Russia) 25, no. 3 (2023): 551–56. http://dx.doi.org/10.15789/1563-0625-pao-2779.

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It is known that there are individual differences in resistance to hypoxia, which can determine the predisposition to the development and severity of various diseases, including infectious, inflammatory and tumor. There are no standardized methods for assessing resistance to hypoxia in experimental animals and humans without hypoxic exposure. The search for molecular-biological markers, identifying people with different resistance to oxygen deficiency under normoxic conditions or under moderate hypoxic exposure is undoubtedly efficient. It is possible that the assessment of the basic resistanc

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O’Leary, Andrew J., Sarah E. Drummond, Deirdre Edge, and Ken D. O’Halloran. "Diaphragm Muscle Weakness Following Acute Sustained Hypoxic Stress in the Mouse Is Prevented by Pretreatment with N-Acetyl Cysteine." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–19. http://dx.doi.org/10.1155/2018/4805493.

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Oxygen deficit (hypoxia) is a major feature of cardiorespiratory diseases characterized by diaphragm dysfunction, yet the putative role of hypoxic stress as a driver of diaphragm dysfunction is understudied. We explored the cellular and functional consequences of sustained hypoxic stress in a mouse model. Adult male mice were exposed to 8 hours of normoxia, or hypoxia (FiO2 = 0.10) with or without antioxidant pretreatment (N-acetyl cysteine, 200 mg/kg i.p.). Ventilation and metabolism were measured. Diaphragm muscle contractile function, myofibre size and distribution, gene expression, protein

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Fletcher, E. C., G. Bao, and C. C. Miller. "Effect of recurrent episodic hypocapnic, eucapnic, and hypercapnic hypoxia on systemic blood pressure." Journal of Applied Physiology 78, no. 4 (1995): 1516–21. http://dx.doi.org/10.1152/jappl.1995.78.4.1516.

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We have described a rat model that responds to chronic (8 h/day, 35 days) repetitive nonapneic episodic (cycled every 30 s) hypocapnic hypoxia with sustained increase in systemic blood pressure. Because the usual blood gas change of apnea is mildly increased CO2, we hypothesized that episodic hypoxia ranging from eucapnea to hypercapnia might cause a greater chronic increase in blood pressure than hypocapnic hypoxia in this model. Five groups of male Sprague-Dawley rats were studied: unhandled group received no treatment, sham group received compressed air in their chambers, hypocapnic hypoxic

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Rytkönen, Kalle T., Gillian M. C. Renshaw, Petra P. Vainio, et al. "Transcriptional responses to hypoxia are enhanced by recurrent hypoxia (hypoxic preconditioning) in the epaulette shark." Physiological Genomics 44, no. 22 (2012): 1090–97. http://dx.doi.org/10.1152/physiolgenomics.00081.2012.

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All animals require molecular oxygen for aerobic energy production, and oxygen availability has played a particularly important role in the evolution of aquatic animals. This study investigates how previous exposure to hypoxia (preconditioning) primes protective transcriptional responses in a hypoxia-tolerant vertebrate species, the epaulette shark ( Hemiscyllium ocellatum). The epaulette shark is a basal cartilaginous fish that in its natural environment experiences cyclic hypoxic periods. We evaluated whether the transcription of a set of crucial prosurvival genes is affected differently by

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Cowburn, Andrew S., Alexi Crosby, David Macias та ін. "HIF2α–arginase axis is essential for the development of pulmonary hypertension". Proceedings of the National Academy of Sciences 113, № 31 (2016): 8801–6. http://dx.doi.org/10.1073/pnas.1602978113.

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Hypoxic pulmonary vasoconstriction is correlated with pulmonary vascular remodeling. The hypoxia-inducible transcription factors (HIFs) HIF-1α and HIF-2α are known to contribute to the process of hypoxic pulmonary vascular remodeling; however, the specific role of pulmonary endothelial HIF expression in this process, and in the physiological process of vasoconstriction in response to hypoxia, remains unclear. Here we show that pulmonary endothelial HIF-2α is a critical regulator of hypoxia-induced pulmonary arterial hypertension. The rise in right ventricular systolic pressure (RVSP) normally

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Itoh, Mai, Yusuke Takahashi, Yuki Okuhashi та Shuji Tohda. "Effects of Hypoxia on HIF, Notch, Akt, and NF-κB Signaling in Leukemia Cell Lines". Blood 122, № 21 (2013): 3874. http://dx.doi.org/10.1182/blood.v122.21.3874.3874.

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Abstract Background Leukemia stem cells reside in the bone marrow niche under hypoxic conditions. The activity of various signaling pathways in the hypoxic environment should be known to understand the pathophysiology of leukemia stem cells. Hypoxia is known to stabilize HIF1α, which transactivates various genes allowing the cell to adapt to hypoxic conditions. Two theories have been reported regarding crosstalk between HIF and Notch signaling; one suggests that HIF1α binds to cleaved Notch1, which results in stabilization of Notch signaling, and the second suggests that HIF1α represses a nega

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Bureau, M. A., A. Cote, P. W. Blanchard, S. Hobbs, P. Foulon, and D. Dalle. "Exponential and diphasic ventilatory response to hypoxia in conscious lambs." Journal of Applied Physiology 61, no. 3 (1986): 836–42. http://dx.doi.org/10.1152/jappl.1986.61.3.836.

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This study was undertaken to test the hypothesis that in the neonate the hypoxic chemoreflex drive adapts to steady-state hypoxia but not to progressive hypoxia. First we have compared the ventilatory (VE) response of 2-day-old conscious lambs to steady-state hypoxia with their response to progressive hypoxia. Second, we have quantified the chemoreceptor excitatory function operating at the end of each period of hypoxia by studying the immediate VE response to the withdrawal of the hypoxic stimulus. Lambs responded to steady-state hypoxia [fractional concentration of inspired O2 (FIO2) = 0.08]

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Massik, J., M. D. Jones, M. Miyabe, et al. "Hypercapnia and response of cerebral blood flow to hypoxia in newborn lambs." Journal of Applied Physiology 66, no. 3 (1989): 1065–70. http://dx.doi.org/10.1152/jappl.1989.66.3.1065.

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Individual effects of hypoxic hypoxia and hypercapnia on the cerebral circulation are well described, but data on their combined effects are conflicting. We measured the effect of hypoxic hypoxia on cerebral blood flow (CBF) and cerebral O2 consumption during normocapnia (arterial PCO2 = 33 +/- 2 Torr) and during hypercapnia (60 +/- 2 Torr) in seven pentobarbital-anesthetized lambs. Analysis of variance showed that neither the magnitude of the hypoxic CBF response nor cerebral O2 consumption was significantly related to the level of arterial PCO2. To determine whether hypoxic cerebral vasodila

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