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Journal articles on the topic 'Intermittent systemic hypoxia'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Artūrs, Paparde, Plakane Līga, and Circenis Kristaps. "Effect of Short Systemic Intermittent Hypoxia on Systemic Hemodynamics Blunted in Cutaneous Microcirculation." Cardiology and Angiology: An International Journal 6, no. 2 (2017): 1–11. https://doi.org/10.9734/CA/2017/33514.

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<strong>Background</strong><strong>:</strong> Hypoxic stimulus induces a homeostatic disruption to enhance physiological adaptation. Blood flow in the microcirculation plays an important role in maintaining healthy tissues by delivering oxygen. The cutaneous microcirculations responses to short systemic hypoxia and especially its duration are poorly understood; however the mechanisms of this phenomenon are at the microcirculatory level. The aim of our study was to determine the short systemic intermittent hypoxia's influence on blood flow in skin, local regulatory mechanism fluctuations and ch

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Torres, Marta, Mauricio Rojas, Noelia Campillo, et al. "Parabiotic model for differentiating local and systemic effects of continuous and intermittent hypoxia." Journal of Applied Physiology 118, no. 1 (2015): 42–47. http://dx.doi.org/10.1152/japplphysiol.00858.2014.

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Hypoxia can be damaging either because cells are directly sensitive to low oxygen pressure in their local microenvironment and/or because they are exposed to circulating factors systemically secreted in response to hypoxia. The conventional hypoxia model, breathing hypoxic air, does not allow one to distinguish between these local and systemic effects. Here we propose and validate a model for differentially applying local and systemic hypoxic challenges in an animal. We used parabiosis, two mice sharing circulation by surgical union through the skin, and tested the hypothesis that when one of

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Hunyor, Imre, and Kristina M. Cook. "Models of intermittent hypoxia and obstructive sleep apnea: molecular pathways and their contribution to cancer." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 4 (2018): R669—R687. http://dx.doi.org/10.1152/ajpregu.00036.2018.

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Obstructive sleep apnea (OSA) is common and linked to a variety of poor health outcomes. A key modulator of this disease is nocturnal intermittent hypoxia. There is striking epidemiological evidence that patients with OSA have higher rates of cancer and cancer mortality. Small-animal models demonstrate an important role for systemic intermittent hypoxia in tumor growth and metastasis, yet the underlying mechanisms are poorly understood. Emerging data indicate that intermittent hypoxia activates the hypoxic response and inflammatory pathways in a manner distinct from chronic hypoxia. However, t

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Fletcher, Eugene C. "Invited Review: Physiological consequences of intermittent hypoxia: systemic blood pressure." Journal of Applied Physiology 90, no. 4 (2001): 1600–1605. http://dx.doi.org/10.1152/jappl.2001.90.4.1600.

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One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles o

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McNulty, P. H., C. Ng, W. X. Liu, et al. "Autoregulation of myocardial glycogen concentration during intermittent hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 2 (1996): R311—R319. http://dx.doi.org/10.1152/ajpregu.1996.271.2.r311.

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During hypoxia, the heart consumes glycogen to generate ATP. Tolerance of repetitive hypoxia logically requires prompt replenishment of glycogen, a process whose regulation is not fully understood. To examine this, we imposed a defined hypoxic stimulus on the rat heart while varying its workload. In intact rats, hypoxia reduced myocardial glycogen approximately 30% and increased both the fraction of glycogen synthase in its physiologically active (GS I) form (from 0.24 +/- 0.06 to 0.82 +/- 0.07; P < 0.005) and glycogen synthesis (from 0.087 +/- 0.011 to 0.375 +/- 0.046 mumol.g-1.min-1; P &l

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Zhang, Jing, Xu Guo, Yanwei Shi, Jing Ma, and Guangfa Wang. "Intermittent hypoxia with or without hypercapnia is associated with tumorigenesis by decreasing the expression of brain derived neurotrophic factor and miR-34a in rats." Chinese Medical Journal 127, no. 1 (2014): 43–47. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20131683.

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Background Very recent studies revealed that obstructive sleep apnoea (OSA) is a contributor of the increased incidence and mortality of cancer in humans, but mechanisms of how OSA promotes tumorigenesis remains largely unknown. We investigated whether intermittent hypoxia with and without hypercapnia plays a role in tumorigenesis. Methods First, Sprague-Dawley (SD) male rats (12 weeks old) were subjected to different hypoxia exposures: intermittent hypoxia and intermittent hypoxia with hypercapnia; continuous hypoxia and normal air. The systemic application of chronic fast rate hypoxia with o

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Reinke, Christian, Shannon Bevans-Fonti, Luciano F. Drager, Mi-Kyung Shin, and Vsevolod Y. Polotsky. "Effects of different acute hypoxic regimens on tissue oxygen profiles and metabolic outcomes." Journal of Applied Physiology 111, no. 3 (2011): 881–90. http://dx.doi.org/10.1152/japplphysiol.00492.2011.

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Obstructive sleep apnea (OSA) causes intermittent hypoxia (IH) during sleep. Both obesity and OSA are associated with insulin resistance and systemic inflammation, which may be attributable to tissue hypoxia. We hypothesized that a pattern of hypoxic exposure determines both oxygen profiles in peripheral tissues and systemic metabolic outcomes, and that obesity has a modifying effect. Lean and obese C57BL6 mice were exposed to 12 h of intermittent hypoxia 60 times/h (IH60) [inspired O2 fraction (FiO2) 21–5%, 60/h], IH 12 times/h (FiO2 5% for 15 s, 12/h), sustained hypoxia (SH; FiO2 10%), or no

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Peng, Ying-Jie, and Nanduri R. Prabhakar. "Effect of two paradigms of chronic intermittent hypoxia on carotid body sensory activity." Journal of Applied Physiology 96, no. 3 (2004): 1236–42. http://dx.doi.org/10.1152/japplphysiol.00820.2003.

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Reflexes arising from the carotid bodies may play an important role in cardiorespiratory changes evoked by chronic intermittent hypoxia (CIH). In the present study, we examined whether CIH affects the hypoxic sensing ability of the carotid bodies and, if so, by what mechanisms. Experiments were performed on adult male rats (Sprague-Dawley, 250–300 g) exposed to two paradigms of CIH for 10 days: 1) multiple exposures to short durations of intermittent hypoxia per day (SDIH; 15sof5%O2 + 5 min of 21% O2, 9 episodes/h, 8 h/day) and 2) single exposure to longer durations of intermittent hypoxia per

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Iturriaga, Rodrigo, Rodrigo Del Rio, and Julio Alcayaga. "Carotid Body Inflammation: Role in Hypoxia and in the Anti-inflammatory Reflex." Physiology 37, no. 3 (2022): 128–40. http://dx.doi.org/10.1152/physiol.00031.2021.

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Emergent evidence indicates that the carotid body (CB) chemoreceptor may sense systemic inflammatory molecules and is an afferent arm of the anti-inflammatory reflex. Moreover, a proinflammatory milieu within the CB is involved in the enhanced CB chemosensory responsiveness to oxygen following sustained and intermittent hypoxia. In this review, we focus on the physiopathological participation of CBs in inflammatory diseases, such as sepsis and intermittent hypoxia.

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Uzun, Andreea-Bianca, Mădălina Gabriela Iliescu, Liliana-Elena Stanciu, et al. "Effectiveness of Intermittent Hypoxia–Hyperoxia Therapy in Different Pathologies with Possible Metabolic Implications." Metabolites 13, no. 2 (2023): 181. http://dx.doi.org/10.3390/metabo13020181.

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Intermittent oxygen therapy (IHT), initially used in the hypoxic administration variant, has been shown to be effective in various pathologies studied, from cardiopulmonary to vascular and metabolic pathologies and more. IHT used to prevent and treat various diseases has thus gained more and more attention as the years have passed. The mechanisms underlying the beneficial effects have been investigated at multiple biological levels, from systemic physiological reactions to genomic regulation. In the last decade, a new method of intermittent oxygen therapy has been developed that combines hypox

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Semenza, Gregg L. "Regulation of Oxygen Homeostasis by Hypoxia-Inducible Factor 1." Physiology 24, no. 2 (2009): 97–106. http://dx.doi.org/10.1152/physiol.00045.2008.

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Metazoan organisms are dependent on a continuous supply of O2 for survival. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that regulates oxygen homeostasis and plays key roles in development, physiology, and disease. HIF-1 activity is induced in response to continuous hypoxia, intermittent hypoxia, growth factor stimulation, and Ca2+ signaling. HIF-1 mediates adaptive responses to hypoxia, including erythropoiesis, angiogenesis, and metabolic reprogramming. In each case, HIF-1 regulates the expression of multiple genes encoding key components of the response pathway. HIF-1 also

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Serebrovskaya, Tatiana V., Eugenia B. Manukhina, Michael L. Smith, H. Fred Downey, and Robert T. Mallet. "Intermittent Hypoxia: Cause of or Therapy for Systemic Hypertension?" Experimental Biology and Medicine 233, no. 6 (2008): 627–50. http://dx.doi.org/10.3181/0710-mr-267.

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Campen, M. J., L. A. Shimoda, and C. P. O’Donnell. "Acute and chronic cardiovascular effects of intermittent hypoxia in C57BL/6J mice." Journal of Applied Physiology 99, no. 5 (2005): 2028–35. http://dx.doi.org/10.1152/japplphysiol.00411.2005.

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We investigated the effects of 1) acute hypoxia and 2) 5 wk of chronic intermittent hypoxia (IH) on the systemic and pulmonary circulations of C57BL/6J mice. Mice were chronically instrumented with either femoral artery or right ventricular catheters. In response to acute hypoxia (4 min of 10% O2; n = 6), systemic arterial blood pressure fell ( P < 0.005) from 107.7 ± 2.5 to 84.7 ± 6.5 mmHg, whereas right ventricular pressure increased ( P < 0.005) from 11.7 ± 0.8 to 14.9 ± 1.3 mmHg. Another cohort of mice was then exposed to IH for 5 wk (O2 nadir = 5%, 60-s cycles, 12 h/day) and then im

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Fletcher, E. C., J. Lesske, R. Behm, C. C. Miller, H. Stauss, and T. Unger. "Carotid chemoreceptors, systemic blood pressure, and chronic episodic hypoxia mimicking sleep apnea." Journal of Applied Physiology 72, no. 5 (1992): 1978–84. http://dx.doi.org/10.1152/jappl.1992.72.5.1978.

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We have described a rat model that responds to repetitive episodic hypoxia (12-s infusions of nitrogen into daytime sleeping chambers every 30 s, 7 h/day for 35 days) with an increase in diurnal systemic blood pressure. We hypothesized that afferent information from the peripheral chemoreceptors may be necessary to produce diurnal blood pressure elevation in this hypoxia model. Carotid body denervation (CBD) was accomplished by severing both carotid sinus nerves in two groups of male Wistar rats (250–375 g). Group 4 CBD rats were subjected to intermittent hypoxia for 35 days (3–5% nadir ambien

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Paparde, Artūrs, Līga Plakane, and Kristaps Circenis. "Effect of Short Systemic Intermittent Hypoxia on Systemic Hemodynamics Blunted in Cutaneous Microcirculation." Cardiology and Angiology: An International Journal 6, no. 2 (2017): 1–11. http://dx.doi.org/10.9734/ca/2017/33514.

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Nanduri, Jayasri, and R. Prabhakar Nanduri. "Cellular mechanisms associated with intermittent hypoxia." Essays in Biochemistry 43 (August 10, 2007): 91–104. http://dx.doi.org/10.1042/bse0430091.

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Hypoxia, i.e. decreased availability of oxygen occurs under many different circumstances and can be either continuous or intermittent. Continuous hypoxia such as that experienced during periods of high altitude leads to physiological adaptations, whereas chronic IH (intermittent hypoxia) associated with sleep-disordered breathing manifested as recurrent apneas leads to morbidity. The purpose of the present chapter is to highlight recent findings on cellular responses to IH. Studies on cell culture models of IH revealed that for a given duration and intensity, IH is more potent than continuous

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Mallet, Robert T., Eugenia B. Manukhina, Steven Shea Ruelas, James L. Caffrey, and H. Fred Downey. "Cardioprotection by intermittent hypoxia conditioning: evidence, mechanisms, and therapeutic potential." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (2018): H216—H232. http://dx.doi.org/10.1152/ajpheart.00060.2018.

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The calibrated application of limited-duration, cyclic, moderately intense hypoxia-reoxygenation increases cardiac resistance to ischemia-reperfusion stress. These intermittent hypoxic conditioning (IHC) programs consistently produce striking reductions in myocardial infarction and ventricular tachyarrhythmias after coronary artery occlusion and reperfusion and, in many cases, improve contractile function and coronary blood flow. These IHC protocols are fundamentally different from those used to simulate sleep apnea, a recognized cardiovascular risk factor. In clinical studies, IHC improved ex

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Kimura, Hiroshi, Hiroyo Ota, Yuya Kimura, and Shin Takasawa. "Effects of Intermittent Hypoxia on Pulmonary Vascular and Systemic Diseases." International Journal of Environmental Research and Public Health 16, no. 17 (2019): 3101. http://dx.doi.org/10.3390/ijerph16173101.

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Obstructive sleep apnea (OSA) causes many systemic disorders via mechanisms related to sympathetic nerve activation, systemic inflammation, and oxidative stress. OSA typically shows repeated sleep apnea followed by hyperventilation, which results in intermittent hypoxia (IH). IH is associated with an increase in sympathetic activity, which is a well-known pathophysiological mechanism in hypertension and insulin resistance. In this review, we show the basic and clinical significance of IH from the viewpoint of not only systemic regulatory mechanisms focusing on pulmonary circulation, but also c

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Arnaud, Claire, Pauline Béguin, Patrick Lévy, and Jean-Louis Pépin. "Normoxic Recovery Reverses Intermittent Hypoxia-Induced Systemic and Vascular Inflammation." Chest 150, no. 2 (2016): 471–73. http://dx.doi.org/10.1016/j.chest.2016.05.031.

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Mackenzie, R. W. A., and P. Watt. "A Molecular and Whole Body Insight of the Mechanisms Surrounding Glucose Disposal and Insulin Resistance with Hypoxic Treatment in Skeletal Muscle." Journal of Diabetes Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/6934937.

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Although the mechanisms are largely unidentified, the chronic or intermittent hypoxic patterns occurring with respiratory diseases, such as chronic pulmonary disease or obstructive sleep apnea (OSA) and obesity, are commonly associated with glucose intolerance. Indeed, hypoxia has been widely implicated in the development of insulin resistance either via the direct action on insulin receptor substrate (IRS) and protein kinase B (PKB/Akt) or indirectly through adipose tissue expansion and systemic inflammation. Yet hypoxia is also known to encourage glucose transport using insulin-dependent mec

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Fagan, Karen A. "Selected Contribution: Pulmonary hypertension in mice following intermittent hypoxia." Journal of Applied Physiology 90, no. 6 (2001): 2502–7. http://dx.doi.org/10.1152/jappl.2001.90.6.2502.

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Sleep apnea (intermittent periods of hypoxia with or without hypercapnia) is associated with systemic hypertension and increased mortality from cardiovascular disease, but the relationship to pulmonary hypertension is uncertain. Previous studies on intermittent hypoxia (IH) in rats that demonstrated pulmonary hypertension utilized relatively long periods of hypoxia. Recent studies that utilized brief periods of hypoxia have conflicting reports of right ventricular (RV) hypertrophy. In addition, many studies have not measured pulmonary hemodynamics to asses the severity of pulmonary hypertensio

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de Frutos, Sergio, Elizabeth Caldwell, Carlos H. Nitta, et al. "NFATc3 contributes to intermittent hypoxia-induced arterial remodeling in mice." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 2 (2010): H356—H363. http://dx.doi.org/10.1152/ajpheart.00341.2010.

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Sleep apnea (SA) is defined as intermittent respiratory arrest during sleep and affects up to 20% of the adult population. SA is also associated with an increased incidence of hypertension and peripheral vascular disease. Exposing rodents to intermittent hypoxia during sleep mimics the cyclical hypoxia/normoxia of SA. We have previously shown that in mice and rats intermittent hypoxia induces ET-1 upregulation and systemic hypertension. Furthermore, intermittent hypoxia (IH) in mice increases nuclear factor of activated T cells isoform 3 (NFATc3) transcriptional activity in aorta and mesenteri

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Agosto-Marlin, Ibis M., Nicole L. Nichols, and Gordon S. Mitchell. "Adenosine-dependent phrenic motor facilitation is inflammation resistant." Journal of Neurophysiology 117, no. 2 (2017): 836–45. http://dx.doi.org/10.1152/jn.00619.2016.

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Phrenic motor facilitation (pMF), a form of respiratory plasticity, can be elicited by acute intermittent hypoxia (i.e., phrenic long-term facilitation, pLTF) or direct application of drugs to the cervical spinal cord. Moderate acute intermittent hypoxia (mAIH; 3 × 5-min episodes of 35–50 mmHg arterial Po2, 5-min normoxic intervals) induces pLTF by a serotonin-dependent mechanism; mAIH-induced pLTF is abolished by mild systemic inflammation induced by a low dose of lipopolysaccharide (LPS; 100 μg/kg ip). In contrast, severe acute intermittent hypoxia (sAIH; 3 × 5-min episodes of 25–30 mmHg art

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Peng, Ying-Jie, and Nanduri R. Prabhakar. "Reactive oxygen species in the plasticity of respiratory behavior elicited by chronic intermittent hypoxia." Journal of Applied Physiology 94, no. 6 (2003): 2342–49. http://dx.doi.org/10.1152/japplphysiol.00613.2002.

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Long-term facilitation (LTF) of breathing elicited by episodic hypoxia (EH) is an extensively studied example of plasticity of respiratory motor behavior. Previous studies employed the paradigm of EH wherein each episode of hypoxia was 5 min. This paradigm is rarely encountered in nature. Brief episodes of hypoxia are encountered frequently with recurrent apneas, wherein hypoxic episodes last a few seconds only. Recent studies suggest that chronic intermittent hypoxia (CIH) represents a form of oxidative stress involving reactive O2species. The objectives of the present study were to determine

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Farré, Ramon, Isaac Almendros, Miguel-Ángel Martínez-García, and David Gozal. "Experimental Models to Study End-Organ Morbidity in Sleep Apnea: Lessons Learned and Future Directions." International Journal of Molecular Sciences 23, no. 22 (2022): 14430. http://dx.doi.org/10.3390/ijms232214430.

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Sleep apnea (SA) is a very prevalent sleep breathing disorder mainly characterized by intermittent hypoxemia and sleep fragmentation, with ensuing systemic inflammation, oxidative stress, and immune deregulation. These perturbations promote the risk of end-organ morbidity, such that SA patients are at increased risk of cardiovascular, neurocognitive, metabolic and malignant disorders. Investigating the potential mechanisms underlying SA-induced end-organ dysfunction requires the use of comprehensive experimental models at the cell, animal and human levels. This review is primarily focused on t

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Prabhakar, Nanduri R., Ganesh K. Kumar, Jayasri Nanduri, and Gregg L. Semenza. "ROS Signaling in Systemic and Cellular Responses to Chronic Intermittent Hypoxia." Antioxidants & Redox Signaling 9, no. 9 (2007): 1397–404. http://dx.doi.org/10.1089/ars.2007.1732.

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Chaddha, Ashish, Oleg Broytman, and Mihaela Teodorescu. "Effects of allergic airway inflammation and chronic intermittent hypoxia on systemic blood pressure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 319, no. 5 (2020): R566—R574. http://dx.doi.org/10.1152/ajpregu.00325.2019.

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Asthma and obstructive sleep apnea (OSA) are highly prevalent chronic conditions, and both are associated with systemic hypertension. Additionally, asthma and OSA reciprocally interact, mutually exacerbating each other. In this study, we tested the effect of allergen-induced lower airway inflammation and concurrent chronic intermittent hypoxia (CIH) on systemic blood pressure (BP), pulmonary function, and proinflammatory cytokines, in a rat model. Brown Norway rats were exposed to 43 days of normoxia (NORM) or CIH, concurrent with weekly house dust mite (HDM) challenges. BP was measured 1 day

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de Frutos, Sergio, Laura Duling, Dominique Alò, et al. "NFATc3 is required for intermittent hypoxia-induced hypertension." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (2008): H2382—H2390. http://dx.doi.org/10.1152/ajpheart.00132.2008.

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Sleep apnea, defined as intermittent respiratory arrest during sleep, is associated with increased incidence of hypertension and peripheral vascular disease. Exposure of rodents to brief periods of intermittent hypercarbia/hypoxia (H-IH) during sleep mimics the cyclical hypoxia-normoxia of sleep apnea. Endothelin-1, an upstream activator of nuclear factor of activated T cells (NFAT), is increased during H-IH. Therefore, we hypothesized that NFATc3 is activated by H-IH and is required for H-IH-induced hypertension. Consistent with this hypothesis, we found that H-IH (20 brief exposures per hour

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Takahashi, Keiko, Takashi Kobayashi, Takeshi Sugaya, et al. "SP081PATHOPHYSIOLOGICAL ROLE OF KIDNEY IN SYSTEMIC OXIDATIVE STRESS DURING CHRONIC INTERMITTENT HYPOXIA." Nephrology Dialysis Transplantation 31, suppl_1 (2016): i112—i113. http://dx.doi.org/10.1093/ndt/gfw158.09.

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Shobatake, Ryogo, Hiroyo Ota, Nobuyuki Takahashi, Satoshi Ueno, Kazuma Sugie, and Shin Takasawa. "The Impact of Intermittent Hypoxia on Metabolism and Cognition." International Journal of Molecular Sciences 23, no. 21 (2022): 12957. http://dx.doi.org/10.3390/ijms232112957.

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Intermittent hypoxia (IH), one of the primary pathologies of sleep apnea syndrome (SAS), exposes cells throughout the body to repeated cycles of hypoxia/normoxia that result in oxidative stress and systemic inflammation. Since SAS is epidemiologically strongly correlated with type 2 diabetes/insulin resistance, obesity, hypertension, and dyslipidemia included in metabolic syndrome, the effects of IH on gene expression in the corresponding cells of each organ have been studied intensively to clarify the molecular mechanism of the association between SAS and metabolic syndrome. Dementia has rece

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Huxtable, A. G., S. M. C. Smith, S. Vinit, J. J. Watters, and G. S. Mitchell. "Systemic LPS induces spinal inflammatory gene expression and impairs phrenic long-term facilitation following acute intermittent hypoxia." Journal of Applied Physiology 114, no. 7 (2013): 879–87. http://dx.doi.org/10.1152/japplphysiol.01347.2012.

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Although systemic inflammation occurs in most pathological conditions that challenge the neural control of breathing, little is known concerning the impact of inflammation on respiratory motor plasticity. Here, we tested the hypothesis that low-grade systemic inflammation induced by lipopolysaccharide (LPS, 100 μg/kg ip; 3 and 24 h postinjection) elicits spinal inflammatory gene expression and attenuates a form of spinal, respiratory motor plasticity: phrenic long-term facilitation (pLTF) induced by acute intermittent hypoxia (AIH; 3, 5 min hypoxic episodes, 5 min intervals). pLTF was abolishe

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Díaz-García, Elena, Sara García-Tovar, Enrique Alfaro, et al. "Inflammasome Activation: A Keystone of Proinflammatory Response in Obstructive Sleep Apnea." IBJ Plus 1, s5 (2022): 12. http://dx.doi.org/10.24217/2531-0151.22v1s5.00012.

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Introduction: As the mechanism that links obstructive sleep apnea (OSA) with the regulation of inflammatory response is not well known, it is important to understand the inflammasome activation, mainly of NLRP3 (nucleotide-binding oligomerization domain-like receptor 3).To assess the NLRP3 activity in patients with severe OSA and to identify its role in the systemic inflammatory response of patients with OSA. Materials and Methods: We analyzed the NLRP3 activity as well as key components of the inflammasome cascade, such as adaptor molecule apoptosis-associated speck-like protein, caspase-1, G

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Badran, Mohammad, Bisher Abuyassin, Saeid Golbidi, Najib Ayas, and Ismail Laher. "Alpha Lipoic Acid Improves Endothelial Function and Oxidative Stress in Mice Exposed to Chronic Intermittent Hypoxia." Oxidative Medicine and Cellular Longevity 2019 (April 9, 2019): 1–13. http://dx.doi.org/10.1155/2019/4093018.

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Objective. Obstructive sleep apnea (OSA) is characterized by recurrent airway collapse that causes chronic intermittent hypoxia (CIH). OSA is associated with systemic inflammation and oxidative stress resulting in endothelial dysfunction and cardiovascular disease (CVD). Alpha lipoic acid (ALA) is a potent antioxidant with anti-inflammatory properties. We hypothesized that dietary ALA can improve endothelial function of mice exposed to CIH. Methods. Mice were exposed to either CIH or intermittent air (IA) and treated with dietary ALA (0.2% w/w) or a regular chow diet for 8 weeks. Endothelial f

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Nanduri, Jayasri, Ning Wang, Benjamin L. Wang та Nanduri R. Prabhakar. "Lysine demethylase KDM6B regulates HIF-1α-mediated systemic and cellular responses to intermittent hypoxia". Physiological Genomics 53, № 9 (2021): 385–94. http://dx.doi.org/10.1152/physiolgenomics.00045.2021.

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Intermittent hypoxia (IH) is a hallmark manifestation of obstructive sleep apnea (OSA). Rodents treated with IH exhibit hypertension. Hypoxia-inducible factor (HIF)-1-dependent transcriptional activation of NADPH oxidases ( Nox) and the resulting increase in reactive oxygen species (ROS) levels is a major molecular mechanism underlying IH/OSA-induced hypertension. Jumanji C (JmjC)-containing histone lysine demethylases (JmjC-KDMs) are coactivators of HIF-1-dependent transcriptional activation. In the present study, we tested the hypothesis that JmjC-KDMs are required for IH-evoked HIF-1 transc

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Jun, Jonathan, Vladimir Savransky, Ashika Nanayakkara, et al. "Intermittent hypoxia has organ-specific effects on oxidative stress." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 4 (2008): R1274—R1281. http://dx.doi.org/10.1152/ajpregu.90346.2008.

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Obstructive sleep apnea is characterized by upper airway collapse, leading to intermittent hypoxia (IH). It has been postulated that IH-induced oxidative stress may contribute to several chronic diseases associated with obstructive sleep apnea. We hypothesize that IH induces systemic oxidative stress by upregulating NADPH oxidase, a superoxide-generating enzyme. NADPH oxidase is regulated by a cytosolic p47phox subunit, which becomes phosphorylated during enzyme activation. Male C57BL/6J mice were exposed to IH with an inspired O2 fraction nadir of 5% 60 times/h during the 12-h light phase (9

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Prieto-Lloret, Jesus, Elena Olea, Ana Gordillo-Cano, et al. "Maladaptive Pulmonary Vascular Responses to Chronic Sustained and Chronic Intermittent Hypoxia in Rat." Antioxidants 11, no. 1 (2021): 54. http://dx.doi.org/10.3390/antiox11010054.

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Chronic sustained hypoxia (CSH), as found in individuals living at a high altitude or in patients suffering respiratory disorders, initiates physiological adaptations such as carotid body stimulation to maintain oxygen levels, but has deleterious effects such as pulmonary hypertension (PH). Obstructive sleep apnea (OSA), a respiratory disorder of increasing prevalence, is characterized by a situation of chronic intermittent hypoxia (CIH). OSA is associated with the development of systemic hypertension and cardiovascular pathologies, due to carotid body and sympathetic overactivation. There is

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Zhang, Yi, Ning Zhong, Jiying Gia, and Zhaonian Zhou. "Effects of Chronic Intermittent Hypoxia on the Hemodynamics of Systemic Circulation in Rats." Japanese Journal of Physiology 54, no. 2 (2004): 171–74. http://dx.doi.org/10.2170/jjphysiol.54.171.

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Wu, Chun-xiao, Yue Liu, and Jing-chun Zhang. "Chronic intermittent hypoxia and hypertension: A review of systemic inflammation and Chinese Medicine." Chinese Journal of Integrative Medicine 19, no. 5 (2013): 394–400. http://dx.doi.org/10.1007/s11655-013-1459-x.

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Prabhakar, Nanduri R., Thomas E. Dick, Jayasri Nanduri, and Ganesh K. Kumar. "Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia." Experimental Physiology 92, no. 1 (2007): 39–44. http://dx.doi.org/10.1113/expphysiol.2006.036434.

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Aron-Wisnewsky, Judith, Caroline Minville, Joan Tordjman, et al. "Chronic intermittent hypoxia is a major trigger for non-alcoholic fatty liver disease in morbid obese." Journal of Hepatology 56, no. 1 (2011): 225–33. https://doi.org/10.1016/j.jhep.2011.04.022.

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Background & Aims Morbid obesity is frequently associated with low grade systemic inflammation, increased macrophage accumulation in adipose tissue (AT), obstructive sleep apnea (OSA), and nonalcoholic fatty liver disease (NAFLD). It has been suggested that chronic intermittent hypoxia (CIH) resulting from OSA could be an independent factor for early stage of NAFLD in addition to other well-recognized factors (dyslipidemia or insulin resistance). Moreover, macrophage accumulation in AT is associated with local hypoxia in fat tissue. We hypothesized that the association between CIH and morb

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Drager, Luciano F., Vsevolod Y. Polotsky, Christopher P. O'Donnell, Sergio L. Cravo, Geraldo Lorenzi-Filho, and Benedito H. Machado. "Translational approaches to understanding metabolic dysfunction and cardiovascular consequences of obstructive sleep apnea." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 7 (2015): H1101—H1111. http://dx.doi.org/10.1152/ajpheart.00094.2015.

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Obstructive sleep apnea (OSA) is known to be independently associated with several cardiovascular diseases including hypertension, myocardial infarction, and stroke. To determine how OSA can increase cardiovascular risk, animal models have been developed to explore the underlying mechanisms and the cellular and end-organ targets of the predominant pathophysiological disturbance in OSA–intermittent hypoxia. Despite several limitations in translating data from animal models to the clinical arena, significant progress has been made in our understanding of how OSA confers increased cardiovascular

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Kanagy, Nancy L., Benjimen R. Walker, Gary M. Malvin, and Leif D. Nelin. "Intermittent Hypoxia Leads to Endothelin-Dependent Hypertension in a Rat Model of Sleep Apnea." Hypertension 36, suppl_1 (2000): 678. http://dx.doi.org/10.1161/hyp.36.suppl_1.678-a.

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2 Clinical studies of sleep apnea demonstrate that the associated hypoxia/hypercapnia (IH) causes systemic hypertension. Additional studies have found that patients with sleep apnea have elevated plasma levels of endothelin. We hypothesized that IH causes sustained hypertension by increasing endothelin production. Three days after surgery to implant arterial and venous catheters, rats were placed in chambers flushed with room air for 90 secs (21% O 2 /0% CO 2 ) followed by 90 secs hypoxic/hypercapnic air (5% O 2 /5% CO 2 ). This cycle was repeated throughout an 8 hr daily exposure period. Mean

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Shi, Xiangrong, Xiaoli Liu, Diqun Xu, Sarah Ross, James Hall, and Sid O’Bryant. "Normobaric Intermittent Hypoxia Increases Middle Cerebral Arterial Blood Flow Velocity With No Systemic Hypertension." Medicine & Science in Sports & Exercise 49, no. 5S (2017): 61. http://dx.doi.org/10.1249/01.mss.0000516992.99870.3c.

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Minoves, Mélanie, Florence Hazane-Puch, Giorgia Moriondo, et al. "Differential Impact of Intermittent vs. Sustained Hypoxia on HIF-1, VEGF and Proliferation of HepG2 Cells." International Journal of Molecular Sciences 24, no. 8 (2023): 6875. http://dx.doi.org/10.3390/ijms24086875.

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Obstructive sleep apnea (OSA) is an emerging risk factor for cancer occurrence and progression, mainly mediated by intermittent hypoxia (IH). Systemic IH, a main landmark of OSA, and local sustained hypoxia (SH), a classical feature at the core of tumors, may act separately or synergistically on tumor cells. Our aim was to compare the respective consequences of intermittent and sustained hypoxia on HIF-1, endothelin-1 and VEGF expression and on cell proliferation and migration in HepG2 liver tumor cells. Wound healing, spheroid expansion, proliferation and migration were evaluated in HepG2 cel

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Dempsey, Jerome A., Frank L. Powell, Gerald E. Bisgard, Gregory M. Blain, Marc J. Poulin, and Curtis A. Smith. "Role of chemoreception in cardiorespiratory acclimatization to, and deacclimatization from, hypoxia." Journal of Applied Physiology 116, no. 7 (2014): 858–66. http://dx.doi.org/10.1152/japplphysiol.01126.2013.

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During sojourn to high altitudes, progressive time-dependent increases occur in ventilation and in sympathetic nerve activity over several days, and these increases persist upon acute restoration of normoxia. We discuss evidence concerning potential mediators of these changes, including the following: 1) correction of alkalinity in cerebrospinal fluid; 2) increased sensitivity of carotid chemoreceptors; and 3) augmented translation of carotid chemoreceptor input (at the level of the central nervous system) into increased respiratory motor output via sensitization of hypoxic sensitive neurons i

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Tkacova, Ruzena, Walter T. McNicholas, Martin Javorsky, et al. "Nocturnal intermittent hypoxia predicts prevalent hypertension in the European Sleep Apnoea Database cohort study." European Respiratory Journal 44, no. 4 (2014): 931–41. http://dx.doi.org/10.1183/09031936.00225113.

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Systemic hypertension is associated with obstructive sleep apnoea syndrome (OSAS) but the pathophysiological mechanisms are incompletely understood. A collaborative European network of 24 sleep centres established a European Sleep Apnoea Database to evaluate cardiovascular morbidity associated with OSAS.11 911 adults referred with suspected OSAS between March 2007 and September 2013 underwent overnight sleep studies, either cardiorespiratory polygraphy or polysomnography. We compared the predictive value of the apnoea–hypopnoea index (AHI) and 4% oxygen desaturation index (ODI) for prevalent h

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Dale, E. A., F. Ben Mabrouk, and G. S. Mitchell. "Unexpected Benefits of Intermittent Hypoxia: Enhanced Respiratory and Nonrespiratory Motor Function." Physiology 29, no. 1 (2014): 39–48. http://dx.doi.org/10.1152/physiol.00012.2013.

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Intermittent hypoxia (IH) is most often thought of for its role in morbidity associated with sleep-disordered breathing, including central nervous system pathology. However, recent evidence suggests that the nervous system fights back in an attempt to minimize pathology by increasing the expression of growth/trophic factors that confer neuroprotection and neuroplasticity. For example, even modest (“low dose”) IH elicits respiratory motor plasticity, increasing the strength of respiratory contractions and breathing. These low IH doses upregulate hypoxia-sensitive growth/trophic factors within r

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McGuire, Michelle, Yi Zhang, David P. White, and Liming Ling. "Serotonin receptor subtypes required for ventilatory long-term facilitation and its enhancement after chronic intermittent hypoxia in awake rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 2 (2004): R334—R341. http://dx.doi.org/10.1152/ajpregu.00463.2003.

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Respiratory long-term facilitation (LTF), a serotonin-dependent, persistent augmentation of respiratory activity after episodic hypoxia, is enhanced by pretreatment of chronic intermittent hypoxia (CIH; 5 min 11-12% O2-5 min air, 12 h/night for 7 nights). The present study examined the effects of methysergide (serotonin 5-HT1,2,5,6,7 receptor antagonist), ketanserin (5-HT2 antagonist), or clozapine (5-HT2,6,7 antagonist) on both ventilatory LTF and the CIH effect on ventilatory LTF in conscious male adult rats to determine which specific receptor subtype(s) is involved. In untreated rats (i.e.

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Hung, Ming-Wai, Gennadi M. Kravtsov, Chi-Fai Lau, Angela Ming-See Poon, George L. Tipoe, and Man-Lung Fung. "Melatonin ameliorates endothelial dysfunction, vascular inflammation, and systemic hypertension in rats with chronic intermittent hypoxia." Journal of Pineal Research 55, no. 3 (2013): 247–56. http://dx.doi.org/10.1111/jpi.12067.

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Moya, Esteban A., Paulina Arias, Carlos Varela, María P. Oyarce, Rodrigo Del Rio, and Rodrigo Iturriaga. "Intermittent Hypoxia-Induced Carotid Body Chemosensory Potentiation and Hypertension Are Critically Dependent on Peroxynitrite Formation." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/9802136.

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Oxidative stress is involved in the development of carotid body (CB) chemosensory potentiation and systemic hypertension induced by chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea. We tested whether peroxynitrite (ONOO−), a highly reactive nitrogen species, is involved in the enhanced CB oxygen chemosensitivity and the hypertension during CIH. Accordingly, we studied effects of Ebselen, an ONOO−scavenger, on 3-nitrotyrosine immunoreactivity (3-NT-ir) in the CB, the CB chemosensory discharge, and arterial blood pressure (BP) in rats exposed to CIH. Male Sprague-D

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