TY - JOUR. T1 - Intermittent hypoxic training protects canine myocardium from infarction. AU - Zong, Pu. AU - Setty, Srinath. AU - Sun, Wei. AU - Martinez, Rodolfo. AU - Tune, Johnathan D.. AU - Ehrenburg, Igor V.. AU - Tkatchouk, Elena N.. AU - Mallet, Robert T.. AU - Downey, H. Fred. PY - 2004/9. Y1 - 2004/9. N2 - This investigation examined cardiac protective effects of normobaric intermittent hypoxia training. Six dogs underwent intermittent hypoxic training for 20 consecutive days in a normobaric chamber ventilated intermittently with N2 to reduce fraction of inspired oxygen (FIO2) to 9.5%-10%. Hypoxic periods, initially 5 mins and increasing to 10 mins, were followed by 4-min normoxic periods. This hypoxia-normoxia protocol was repeated, initially 5 times and increasing to 8 times. The dogs showed no discomfort during intermittent hypoxic training. After 20 days of hypoxic training, the resistance of ventricular myocardium to infarction was assessed in an acute experiment. The left ...
TY - JOUR. T1 - Acute intermittent hypoxia exposures enhance arterial oxygen delivery. AU - Zhang, Peizhen. AU - Downey, H. Fred. AU - Shi, Xiangrong. PY - 2010/9. Y1 - 2010/9. N2 - Physiological adaptations to intermittent hypoxia (IH) conditioning are based on the cumulative effect of repeated IH exposures. The present study sought to test the hypothesis that acute IH exposures would promote arterial O2 delivery and regional tissue oxygenation. Changes in arterial O2 saturation (SaO2, oximeter), forearm muscle and cerebral tissue oxygenations (SmO2 and ScO2, near-infrared spectroscopy) were compared during five repeated hypoxia exposures (10±0.2% O2 for 5-min each) interposed with four-minute inhalation of room air in 11 healthy subjects (24±0.9 y). Baseline, prehypoxia partial pressure of end-tidal O2 (PETO 2, mass spectrometer) and SaO2 (107±2 mmHg and 97.3±0.3%) were decreased (P, 0.05) after the first bout as compared with those during normoxia prior to the second (94±2 mmHg and ...
Intermittent hypoxia-induced changes in tumor-associated macrophages and tumor malignancy in a mouse model of sleep apnea.: Our findings support the notion that
The time course of the pulmonary vascular response to hypoxia in humans has not been fully defined. In this investigation, study A was designed to assess the form of the increase in pulmonary vascular tone at the onset of hypoxia and to determine whether a steady plateau ensues over the following approximately 20 min. Twelve volunteers were exposed twice to 5 min of isocapnic euoxia (end-tidal Po(2) = 100 Torr), 25 min of isocapnic hypoxia (end-tidal Po(2) = 50 Torr), and finally 5 min of isocapnic euoxia. Study B was designed to look for the onset of a slower pulmonary vascular response, and, if possible, to determine a latency for this process. Seven volunteers were exposed to 5 min of isocapnic euoxia, 105 min of isocapnic hypoxia, and finally 10 min of isocapnic euoxia. For both studies, control protocols consisting of isocapnic euoxia were undertaken. Doppler echocardiography was used to measure cardiac output and the maximum tricuspid pressure gradient during systole, and estimates of pulmonary
Breast cancer is the most common cancer in women worldwide and the second most common cancer overall. The most aggressive and most lethal form of breast cancer is inflammatory breast cancer (IBC). The mechanisms underlying the aggressiveness of IBC are still poorly understood. A key feature in the development and progression of breast cancer is the tumor microenvironment that is, amongst others, characterized by a specific composition of the extracellular matrix (ECM) and by the occurrence of tissue hypoxia and oxidative stress. Due to vascular remodeling, leading to structurally and functionally abnormal tumor vessels, tumor cells are exposed to alternating periods of hypoxia and reoxygenation, called chronic intermittent hypoxia (CIH). CIH is a cause of increased reactive oxygen species (ROS) production and has been identified as an important factor in promoting tumor progression and metastasis. However, the molecular mechanisms through which CIH increases the aggressiveness of breast cancer ...
The specificity of computed tomography (CT) for subarachnoid haemorrhage (SAH) is very high. However, physicians should be aware of rare false positive findings, also referred to as pseudo-SAH. We present an unusual case in which such a finding was caused by chronic hypoxaemia. A 37-year-old male patient presented with headaches. His CT-scan showed multiple confluent subarachnoid hyperattenuations, which mimicked SAH. However, the headache was chronic and had no features typical for SAH. The patient suffered from severe chronic hypoxaemia due to congenital heart failure. On CT-angiography diffuse intracranial vessel proliferation was found and laboratory results revealed a highly raised level of haematocrit, which had both probably developed as compensatory mechanisms. A combination of these findings explained the subarachnoid hyperdensities. Magnetic resonance imaging (MRI) showed no signs of SAH and visualized hypoxaemia in cerebral veins. A diagnosis of pseudo-SAH was made. The patients symptoms
Intermittent hypoxia often occurs in early infancy in both preterm and term infants and especially at 36 to 44 weeks postmenstrual age. These episodes of intermittent hypoxia could result from sleep-disordered breathing or may be temporally unrelated to apnea or bradycardia events. There are numerous reports indicating adverse effects of intermittent hypoxia on development, behavior, academic achievement and cognition in children with sleep apnea syndrome. It remains uncertain the exact causative relationship between the neurocognitive and behavioral morbidities and intermittent hypoxia and/or its associated sleep fragmentation. On the other hand, well-controlled and moderate intermittent hypoxia conditioning/training has been used in sick children for treating their various forms of bronchial asthma, allergic dermatoses, autoimmune thyroiditis, cerebral palsy, and obesity. This review article provides an updated and impartial analysis on the currently available evidence in supporting either side of the
Intermittent hypoxia (IH) is believed to contribute to the pathogenesis of hypertension in obstructive sleep apnea through mechanisms that include activation of the renin-angiotensin system. The objective of this study was to assess the role of the t
Fingerprint Dive into the research topics of Hyperoxia and moderate hypoxia fail to affect inspiratory muscle fatigue in humans. Together they form a unique fingerprint. ...
OBJECTIVE: Recently, we showed that 5 days of normobaric intermittent hypoxia at rest (IH; 2 hours daily at 3,800 m simulated altitude; partial pressure of inspired oxygen 90 torr) can induce an increase in the isocapnic hypoxic ventilatory response
The study is a prospective field evaluation to assess the effects of the chronic Intermittent Hypoxia exposure in 12 healthy humans.. Precisely, the study was designed to :. Set up a new model of Chronic Intermittent Hypoxia (CIH) applied to healthy human. This CIH is mimicking the CIH undergone by patients suffering from Sleep Apnea Syndrome.. Evaluate the cardiovascular effect of CIH. Neuronal and humoral sympathetic control, blood pressure control, vascular resistance.. Evaluate the Sleep quality, the ventilation under exposure and the long terms effect on ventilation control of CIH (central and peripheral chemoreflex).. Investigates the biological aspects of CIH exposure. ...
The hormonal responses to submaximal exercise under normoxic and hypoxic conditions were studied in eight fit males, aged 22--28 yr, with mean maximal oxygen uptake of 4.4 +/- 0.7 l/min. Studies were performed in a hypobaric chamber, decompressed to a simulated altitude of 4,550 m (PIO2 = 83 Torr). The subjects exercised for 20 min at 750 kpm/min on a cycle ergometer. Venous blood samples were obtained at rest, during exercise and for 60 min after exercise. Plasma glucose, free fatty acids, lactate, cortisol, and serum growth hormone concentrations all increased more during hypoxic exercise than under normoxic conditions. Serum insulin concentration showed a small decrease under normoxic conditions, but decreased by 50% during hypoxic exercise, and was followed by marked rebound when exercise stopped. These changes suggest that energy substrate-hormone interrelationships are altered by hypoxic exercise, resulting in increased fat mobilization and increased gluconeogenesis.
Regional alveolar hypoxia in the lung induces regional pulmonary vasoconstriction which diverts blood flow from the hypoxic area. However, the predominant determinant of the distribution of perfusion in the normal erect lung is gravity so that more perfusion occurs at the base than at the apex. To determine the strength of the regional alveolar hypoxic response in diverting flow with or against the gravity gradient a divided tracheal cannula was placed in anesthetized dogs and unilateral alveolar hypoxia created by venilating one lung with nitrogen while ventilating the other lung with oxygen to preserve normal systemic oxygentation. Scintigrams of the distribution of perfusion obtained with intravenous 13-N and the MGH positron camera revealed a 34 and 32 per cent decrease in perfusion to the hypoxic lung in the supine and erect positions and a 26 per cent decrease in the decubitus position with the hypoxic lung dependent (P equal to 0.94 from supine shift), indicating nearly equal vasoconstriction
Pulmonary hypertension (PH) and right ventricular (RV) hypertrophy frequently develop in patients with hypoxic lung disease. Chronic alveolar hypoxia (CH) promotes sustained pulmonary vasoconstriction and pulmonary artery (PA) remodeling by acting on lung cells, resulting in the development of PH. RV hypertrophy develops in response to PH, but arterial hypoxemia in CH may influence that response by activating Hypoxia-Inducible Factor-1α (HIF-1α) and/or HIF-2α in cardiomyocytes. Indeed, other studies show that attenuation of PH in CH fails to prevent RV remodeling, suggesting that PH-independent factors regulate RV hypertrophy. Therefore, we examined the role of HIFs in RV remodeling in CH-induced PH. We deleted HIF-1α and/or HIF-2α in hearts of adult mice that were then housed under normoxia or CH (10% O2) for 4 weeks. RNA-seq analysis of the RV revealed that HIF-1α and HIF-2α regulate the transcription of largely distinct gene sets during CH. RV systolic pressure (RVSP) increased and RV ...
TY - JOUR. T1 - Age-dependent vulnerability to ischemia-reperfusion injury of cyanotic myocardium in a chronic hypoxic rat model. AU - Fujita, Yasufumi. AU - Ishino, Kozo. AU - Nakanishi, Koji. AU - Fujii, Yasuhiro. AU - Kawada, Masaaki. AU - Sano, Shunji. PY - 2009/11. Y1 - 2009/11. N2 - This study evaluated the effects of chronic hypoxia from birth on the resistance of rat hearts to global ischemia, with special emphasis on the duration of hypoxia. Male Wistar rats were housed from birth for 4 weeks or 8 weeks either in a hypoxic environment (FiO2 = 0.12) or in ambient air (8 animals for each group). Isolated rat hearts were perfused for 40 min with oxygenated Krebs-Henseleit buffer, subjected to 20 min global no-flow ischemia at 37°C, and then underwent 40 min of reperfusion. A non-elastic balloon was inserted into the left ventricle and inflated until the pre-ischemic LVEDP rose to 8mmHg. Cardiac function was measured before and after ischemia. The post-ischemic percent recovery of LVDP in ...
Areas of hypoxia are found in coastal areas worldwide, and have become increasingly widespread. These areas vary in their duration and dissolved oxygen concentration from occasional diurnal hypoxia, as found in Corpus Christi Bay, Texas, seasonal hypoxia as in the northern Gulf of Mexico, to continuous hypoxia as found in oceanic oxygen minimum zones. The effects of exposure to low dissolved oxygen (DO) depend on the duration of exposure, the DO concentration and an organisms tolerance to hypoxic conditions. Most studies have focused on lethal effects of hypoxia by comparing the abundance of benthic organisms and the species composition of benthic communities between hypoxic and normoxic areas. Sub-lethal effects of such as changes in reproduction may occur at less severe hypoxic conditions (by definition), but may still have effects at the population level. The goal of this study is to examine the sub-lethal reproductive effects of low DO on harpacticoid copepods. The life-history traits and ...
Although tumor progression involves genetic and epigenetic alterations to normal cellular biology, the underlying mechanisms of these changes remain obscure. Numerous studies have shown that hypoxia-inducible factor 1α (HIF-1α) is overexpressed in many human cancers and up-regulates a host of hypoxia-responsive genes for cancer growth and survival. We recently identified an alternative mechanism of HIF-1α function that induces genetic alterations by suppressing DNA repair. Here, we show that long-term hypoxia, which mimics the tumor microenvironment, drives a perpetual epithelial-mesenchymal transition (EMT) through up-regulation of the zinc finger E-box binding homeobox protein ZEB2, whereas short-term hypoxia induces a reversible EMT that requires the transcription factor Twist1. Moreover, we show that the perpetual EMT driven by chronic hypoxia depends on HIF-1α induction of genetic alterations rather than its canonical transcriptional activator function. These mesenchymal tumor cells not ...
In the current study, three portions of the ARAS (the dorsal lower ARAS, ventral lower ARAS and upper ARAS) in a patient with impaired consciousness following DPHL caused by CO poisoning were evaluated using DTT. We found that these three portions of the ARAS were injured in both hemispheres: the upper ARAS - decreased neural connectivity to both frontal cortexes, basal forebrains, basal ganglia and thalami, the dorsal lower ARAS - non-reconstruction in the right side and narrowing in the left side and the ventral lower ARAS -non-reconstruction in both sides. We believe that the impaired consciousness in this patient was ascribed to the injury of the three portions of the ARAS.. Many studies have reported abnormality of the white matter including basal ganglia (caudate nucleus, putamen, and globus pallidus) in patients with DPHL using various neuroimaging tools including conventional MRI [5-13]. Neurological manifestations were observed as follows: 1) cognitive impairments - confusion, ...
As solid tumors grow, regions in the tumor become hypoxic because of increased metabolism, heterogeneous and abnormal vasculature delivering oxygen within the tumor, and greater size. In order for the tumor to continue to grow, it depends on survival mechanisms to overcome this hypoxic state, including up-regulation in glycolysis, invasion and metastasis, and angiogenesis, or the growth of new blood vessels. The hypoxia-inducible factor (HIF) transcription factor complex is a major mediator of the cells response to a hypoxic state and a tumors survival mechanism under hypoxia. The complex is composed of the hypoxia-dependent HIF-1α subunit and a constitutively expressed HIF-1α subunit, and it requires the co-activator protein p300 to function. In the presence of oxygen, HIF-1α is rapidly degraded. Under hypoxia, HIF-1α forms a complex with HIF-1α and p300 in the nucleus to up-regulate transcription of pro-survival and angiogenic genes. Targeting this transcription factor complex in tumors ...
Hypoxia increases the proliferation of hCMPCs. hCMPCs were cultured under normoxic and hypoxic conditions for the indicated time intervals. An increase in the n
fr] OBJECTIF: hypoxie cycliques dans les tumeurs proviennent de lhétérogénéité dans le flux de RBC et influence non seulement les cellules tumorales mais également des cellules endothéliales qui tapissent les vaisseaux sanguins tumoraux. Whether pO(2) fluctuations, particularly transient reoxygenation periods, alter the well-known hypoxia-inducible factor (HIF)-dependent gene program is largely unknown. Que Po (2) les fluctuations, en particulier réoxygénation des périodes transitoires, de modifier lhypoxie bien connue-inducible factor (HIF)-programme des gènes dépendant est largement inconnue. EXPERIMENTAL DESIGN: We compared the transcriptomic profiles of endothelial and tumor cells exposed to cyclic hypoxia versus continuous hypoxia to uncover a possible differential effect on angiogenesis and metastases. EXPERIMENTAL DESIGN: Nous avons comparé les profils transcriptomiques de endothéliales et les cellules tumorales exposées à lhypoxie cyclique par rapport à lhypoxie ...
Hypoxia increases transcript levels of enzymes involved in heme biosynthesis, iron-associated and SreA-associated processes. Microarray datasets include three b
BACKGROUND: Exposure to intermittent hypoxia (IH) may enhance cardiac function and protects heart against ischemia-reperfusion (I/R) injury. To elucidate the underlying mechanisms, we developed a cardioprotective IH model that was characterized at hemodynamic, biochemical and molecular levels. METHODS: Mice were exposed to 4 daily IH cycles (each composed of 2-min at 6-8% O2 followed by 3-min reoxygenation for 5 times) for 14 days, with normoxic mice as controls. Mice were then anesthetized and subdivided in various subgroups for analysis of contractility (pressure-volume loop), morphology, biochemistry or resistance to I/R (30-min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion and measurement of the area at risk and infarct size). In some mice, the phosphatidylinositide 3-kinase (PI3K) inhibitor wortmannin was administered (24 µg/kg ip) 15 min before LAD. RESULTS: We found that IH did not induce myocardial hypertrophy; rather both contractility and ...
Ischemia-reperfusion injury (IRI) occurs when there is transient hypoxia due to the obstruction of blood flow (ischemia) followed by a subsequent re-oxygenation of the tissues (reperfusion). In the skin, ischemia-reperfusion ...
Ischemia-reperfusion injury (IRI) occurs when there is transient hypoxia due to the obstruction of blood flow (ischemia) followed by a subsequent re-oxygenation of the tissues (reperfusion). In the skin, ischemia-reperfusion ...
Hielscher A, Qiu C, Porterfield J, Smith Q, Gerecht S. Hypoxia affects the structure of breast cancer cell-derived matrix to support angiogenic responses of endothelial cells (2013) Journal of Carcinogenesis and Mutagenesis doi: 10.4172/2157-2518.S13-005 ...
En Hospitales Nisa somos especialistas en el tratamiento de enfermedades cerebrales como la anoxia. Informacion, Causas y Tratamiento
Hypoxemia and/or hypoxia is a condition in which there is a deficiency of oxygen reaching the tissues. Know about the symptoms, causes, prevention and treatment.
Intermittent hypoxia has been suggested to increase exercise tolerance by enhancing stress resistance and improving oxygen delivery. Because the improvement of exercise tolerance reduces mortality in the elderly with and without coronary artery disease intermittent hypoxia might be a valuable preventive and therapeutic tool. However, controlled studies are lacking. Sixteen males (50-70 years, 8 with and 8 without prior myocardial infarction) were randomly assigned in a double-blind fashion to receive 15 sessions of passive intermittent hypoxia (hypoxia group) or normoxia (control group) within 3 weeks. For the hypoxia group each session consisted of three to five hypoxic (14-10% oxygen) periods (3-5 min) with 3-min normoxic intervals. Controls inhaled only normoxic air in the same way. Exercise tests were performed before and after the 3-week breathing program. After 3 weeks of intermittent hypoxia peak oxygen consumption had increased compared to normoxic conditions (+ 6.2% vs.-3%, p , 0.001). ...
Exposure to perinatal hypoxia results in alteration of the adult pulmonary circulation, which is linked among others to alterations in K(+) channels in pulmonary artery (PA) smooth muscle cells. In particular, large conductance Ca(2+)-activated K(+) (BK(Ca)) channels protein expression and activity were increased in adult PA from mice born in hypoxia compared with controls. We evaluated long-term effects of perinatal hypoxia on the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathway-mediated activation of BK(Ca) channels, using isoproterenol, forskolin, and dibutyryl-cAMP. Whole-cell outward current was higher in pulmonary artery smooth muscle cells from mice born in hypoxia compared with controls. Spontaneous transient outward currents, representative of BK(Ca) activity, were present in a greater proportion in pulmonary artery smooth muscle cells of mice born in hypoxia than in controls. Agonists induced a greater relaxation in PA of mice born in hypoxia compared with controls, and BK
Sleep apnea (SA) affects as many as 20% of the adult population in the United States. It elicits intermittent hypoxia (IH) and causes pulmonary hypertension (PH), however the mechanisms of this PH have not been well studied. IH has been shown to cause polycythemia, pulmonary vascular remodeling and increases in vasoconstrictor reactivity. CO2 supplementation may be protective in the development of PH, therefore we assessed effects of IH with and without CO2 supplementation on indices of PH and pulmonary vasoconstrictor reactivity. IH with CO2 supplementation resulted in eucapnic IH (E-IH) and the lack of polycythemia or vascular remodeling. However, E-IH caused significant right ventricular hypertrophy and increased pulmonary vasoconstrictor reactivity, which was mediated by vascular smooth muscle (VSM) Ca2+ sensitization. We, therefore, sought to determine the mechanism of this enhanced vasoconstrictor reactivity by assessing vasoconstriction and VSM Ca2+ responses to the endothelium-derived
TY - JOUR. T1 - Long-term histological outcome after post-hypoxic treatment with 100% or 40% oxygen in a model of perinatal hypoxic-ischemic brain injury. AU - Grafe, Marjorie. AU - Woodworth, K. Nina. AU - Noppens, Kristin. AU - Perez-Polo, J. Regino. PY - 2008/2. Y1 - 2008/2. N2 - Hypoxic newborns have traditionally been given supplemental oxygen, and until recently, guidelines for neonatal resuscitation recommended that 100% oxygen be used. Exposure to 100% oxygen after hypoxic injury, however, may exacerbate oxidative stress. The current study evaluated the effect of exposure to 100, 40 or 21% oxygen after neonatal hypoxic-ischemic injury on the severity of brain injury after long-term survival. The severity of histological brain injury was not different in animals exposed to 100% oxygen versus room air. Male animals treated with 40% oxygen post-hypoxia had the lowest mean total histology scores, but this was not statistically significant due to the large variation in injury within each ...
During ventilatory acclimatization to hypoxia (VAH), the relationship between ventilation (VE) and end-tidal PCO2 (PETCO2) changes. This study was designed to determine 1) whether these changes can be seen early in VAH and 2) if these changes are present, whether the responses differ between isocapnic and poikilocapnic exposures. Ten healthy volunteers were studied by using three 8-h exposures: 1) isocapnic hypoxia (IH), end-tidal PO2 (PETO2) = 55 Torr and PETCO2 held at the subjects normal prehypoxic value; 2) poikilocapnic hypoxia (PH), PETO2 = 55 Torr; and 3) control (C), air breathing. The VE-PETCO2 relationship was determined in hyperoxia (PETO2 = 200 Torr) before and after the exposures. We found a significant increase in the slopes of VE-PETCO2 relationship after both hypoxic exposures compared with control (IH vs. C, P | 0.01; PH vs. C, P | 0.001; analysis of covariance with pairwise comparisons). This increase was not significantly different between protocols IH and PH. No significant changes
Continuous or intermittent hypobaric hypoxia can lead to long-term contraction of the pulmonary artery and structural changes in the pulmonary vascular wall known as hypoxic pulmonary vessel remodelling (HPVR) [20]. HPVR is characterised by thickening of small pulmonary artery wall and muscularizing of pulmonary arteriole, which can result in sustained high pulmonary artery pressure and right ventricular hypertrophy [21]. It has become clear that pulmonary vascular smooth muscle cells (PASMCs) are closely related to the development of pulmonary hypertension, which are regulated by intracellular Ca2+ concentrations and calmodulin (CaM) [1]. The intracellular Ca2+ concentration has also been suggested to regulate gene expression and cellular proliferation [2, 6, 22-25]. Intracellular calcium levels in PASMCs are mainly regulated by extracellular calcium influx and the release of intracellular calcium stores. Chelation of extracellular calcium in human PASMCs can significantly inhibit serum or ...
Serotonin initiates neuroplasticity in a number of invertebrate and vertebrate experimental models. The first report of serotonin-dependent plasticity in respiratory motor control was a long-lasting facilitation of phrenic activity following episodic stimulation of chemoafferent neurons [1], a phenomenon now known as long-term facilitation (LTF). Recent progress has contributed considerably towards an understanding of the mechanisms and manifestations of this potentially important model of respiratory plasticity. In this presentation, recent progress in understanding the mechanism of LTF will be reviewed. In all studies, we exposed awake or anesthetized Sprague Dawley rats to episodic hypoxia as an experimental model of LTF. Both awake and anesthetized rats express LTF following episodic hypoxia. Intermittent, but not continuous hypoxia elicits LTF, indicating remarkable pattern sensitivity in its underlying mechanism. Both episodic chemoafferent activation by stimulation of the carotid sinus ...
Tissue hypoxia is frequently found under various pathophysiological conditions, such as circulatory failure, myocardial infarction and cerebral ischemia (Garin et al., 2005; Li and Jackson, 2002; McCord, 1985; Michiels, 2004). Owing to the high incidence and clinical relevance of tissue hypoxia and ischemia-reperfusion injury, an understanding of the hypoxia-associated cellular and molecular mechanisms is essential for the development of new and effective strategies to reduce ischemia-reperfusion- and tissue-hypoxia-mediated cell damage.. An elegant and straightforward method for the investigation of hypoxia-associated mechanisms is the use of cell culture systems. So far, different in vitro models (e.g. hypoxic chambers, chemical or enzymatic generation of hypoxia) have been employed to induce hypoxic conditions in cultures of cell lines and primary cells and to evaluate the effects as well as underlying mechanisms of in vitro hypoxia. Unfortunately, all of the currently described models have ...
A hypoxicator is a medical device intended to provide a stimulus for the adaptation of an individuals cardiovascular system by means of breathing reduced oxygen hypoxic air and triggering mechanisms of compensation. The aim of intermittent hypoxic training or hypoxic therapy conducted with such a device is to obtain benefits in physical performance and wellbeing through improved oxygen metabolism. There are several commercial systems available, the most popular being Hypoxico, Inc., who pioneered normobaric hypoxic altitude training systems. Most of these systems have not been cleared for medical applications by the FDA and are used by athletes for altitude training. Advanced hypoxicators have a built-in pulse oximeter used to monitor and in some cases control the temporary reduction of arterial oxygen saturation that results in physiological responses evident at both systemic and cellular levels even after only a few minutes of hypoxia. Hypoxic Training Index (HTi) can be used to measure the ...
This study demonstrates for the first time changes in the expression of HDAC proteins, specifically increased HDAC1 (class I) and HDAC5 (class II), in human IPAH lung. These data were replicated in lungs and RV from rats with hypoxia-induced pulmonary hypertension. The lack of change in HDAC expression in the kidneys from these animals links the observed changes in HDAC expression to the pathological vascular remodeling of pulmonary hypertension rather than the hypoxic stimulus per se. Immunohistochemical assessment of human IPAH and chronic hypoxic rat lungs confirmed increased nuclear expression of HDAC1 and cytoplasmic expression of HDAC5 in remodeled vessels. These vessels also express the proliferative marker Ki67, supporting a link between aberrant epigenetic changes and dysregulated cell proliferation. Consistent with a functional role for HDACs in pulmonary hypertension, long-term administration of VPA, a HDAC class I inhibitor, not only prevented hypoxia-induced pulmonary hypertension ...
1. Six groups of 20 male adult rats were maintained in an environmental chamber, each group for a period of 28 days. One group breathed air throughout its experimental period, and a second group breathed a normobaric atmosphere of 12% oxygen. The other four groups were exposed to this hypoxic atmosphere for only a proportion of each 24 h cycle: 2, 4 and 12 h daily, and eight periods of 30 min daily.. 2. After 28 days, measurement was made, in each rat, of right ventricule (RV) weight and of red cell mass (RCM) by using 51Cr-labelled rat erythrocytes.. 3. In the normoxic control group, RV weight corrected for log body weight in grams was 63.2 ± 1 mg/log body wt. and RCM was 2.02 ± 0.05 ml/100 g body wt. This was significantly less than in the group hypoxic for only 2 h each day for 28 days: RV weight 66.6 ± 0.8 mg/log body wt. (P , 0.05) and RCM 2.27 ± 0.05 ml/100g body wt. (P , 0.05). Greater increases compared with control were observed in all the other hypoxic groups. There was no ...
Results Green fluorescence was observed in the cells transfected of negative control siRNA group though the fluorescence microscope. Compared with the blank control group, The MTT assay determined that the survival rate of H9C2 was decreased (p , 0.05) after the injured by hypoxia. And the results of flow cytometry showed that hypoxia increased cell apoptosis rate (P , 0.01) and the concentration of calcium (p , 0.01), while the transfection of Bim-siRNA reduced the effects caused by hypoxia (P , 0.05 or P , 0.01). Compared with the hypoxia group, the transfection of Bim-siRNA increased the cell survival rate, decreased cell apoptosis rate and the concentration of calcium (p , 0.01 or p , 0.05). While there was no significant difference among Hypoxia Group, Hypoxia + Negative Control siRNA Group and Hypoxia + Mock control Group (p , 0.05). The results of Western blotting showed that the transfection of Bim-siRNA reduced the expression of Bim obviously (p , 0.01); meanwhile, reduced the ...
Pulmonary vascular remodeling is one of the typical responses to chronic alveolar hypoxia in the rat model of pulmonary hypertension (PH). Neither the etiology nor the structural and functional consequences of this remodeling are well understood. It is known that chronic treatment with ACE inhibitors results in a reduction of lung perfusion pressures and vascular changes in hypoxic PH, but the effect of treatment with ACE inhibitors on arterial tree morphology and mechanical properties of the artery walls in the intact lung have not been examined. In addition to using standard hemodynamic analysis, we approach this problem with x-ray micro-CT imaging and measure the distensibility of pulmonary arteries (approximate range of 50 - 2000 um diameter) in rat lungs. We examine consequences of chronic hypoxic exposure (10% O2) with and without Captopril treatment in FH, SD and BN rats. The FH rat strain is known to possess a genetic susceptibility to PH whereas the BN strain is resistant to PH. An example of
p,This study evaluated the effects of chronic hypoxia from birth on the resistance of rat hearts to global ischemia, with special emphasis on the duration of hypoxia. Male Wistar rats were housed from birth for 4 weeks or 8 weeks either in a hypoxic environment (FiO20.12) or in ambient air (8 animals for each group). Isolated rat hearts were perfused for 40 min with oxygenated Krebs-Henseleit buffer, subjected to 20 min global no-flow ischemia at 37, and then underwent 40 min of reperfusion. A non-elastic balloon was inserted into the left ventricle and inflated until the pre-ischemic LVEDP rose to 8mmHg. Cardiac function was measured before and after ischemia. The post-ischemic percent recovery of LVDP in hypoxic hearts was worse than in normoxic hearts (4 weeks:55+/-7 vs. 96+/-3%, p0.01;8 weeks:40+/-5 vs. 92+/-4%, p0.01), and was worst in the 8-week-hypoxic hearts. Similarly, the percent recovery of dP/dt in the hypoxic hearts was lower than in the normoxic hearts (4 weeks:51+/-5 vs. 96+/-7%, ...
NO/cGMP signal transduction plays an important role in the modulation of pulmonary vascular tone and structure in response to acute and chronic changes in oxygen tension. In this study, single aerosol delivery of adenoviral vectors expressing NOS2 and NOS3 gene in rat lungs resulted in immunoreactive NOS2 and NOS3 localized in bronchial and alveolar epithelial cells. NOS gene transfer increased pulmonary cGMP levels and elevated exhaled NO levels for at least 1 week. Significantly higher NO production was observed in NOS2-aerosolized rats than in NOS3- and control virus-infected rats. The acute hypoxia-induced vasoconstrictor response was significantly and equally reduced in both NOS2- and NOS3-infected rats. In contrast, in rats breathing Fio2 0.10 for 1 week, a single administration of AdNOS2 significantly reduced the rise in PAP, the increase in fractional right ventricular weight, and the degree of pulmonary vascular remodeling. In contrast, single administration of AdRR5 or AdNOS3 did not ...
We report that chronic sublethal hypoxia in newborn mice produces an initial 30% deficit in cortical neurons, two-thirds of which are excitatory neurons expressing the transcription factor Tbr1. Over the ensuing 4 weeks in normoxic conditions, the deficit in neuron number recovers, such that neither NeuN+, Tbr1+ nor SMI-32+ neurons are decreased in the cortex of hypoxic-reared mice at P48. However, there is an enduring loss in PV+ and CR+ inhibitory interneurons in the hypoxic mice, which creates an imbalance between excitatory and inhibitory neurons in the hypoxic cortex. Disrupting the Fgfr1 gene in GFAP+ cells of the developing dorsal telencephalon (including cortical radial glial cells and all their progeny) does not alter the initial loss of cortical neurons but precludes the recovery of NeuN+, Tbr1+ and SMI-32+ neuron number in the cerebral cortex. Hypoxic exposure increases cell proliferation and the generation of Tbr1+ cortical excitatory neurons and that of OB granular neurons, ...
Hypoxic exposure lasting a few hours results in an elevation of ventilation and a lowering of end-tidal P(CO2) (P(ET(CO2))) that persists on return to breathing air. We sought to determine whether this increment in ventilation is fixed (hypothesis 1), or whether it increases in proportion to the rise in metabolic rate associated with exercise (hypothesis 2). Ten subjects were studied on two separate days. On 1 day, subjects were exposed to 8h of isocapnic hypoxia (end-tidal P(O2) 55 Torr) and on the other day to 8 h of euoxia as a control. Before and 30 min after each exposure, subjects undertook an incremental exercise test. The best fit of a model for the variation in P(ET(CO2)) with metabolic rate gave a residual squared error that was approximately 20-fold less for hypothesis 2 than for hypothesis 1 (p|0.005, F-ratio test). We conclude that the alterations in respiratory control induced during early ventilatory acclimatization to hypoxia better reflect those associated with hypothesis 2 rather than
It has been generally thought that PH predominantly resulted from hypoxia-induced structural changes in the pulmonary vasculature, which produced a fixed increase in resistance. These structural changes included remodeling of the arteriolar walls leading to encroachment into the vascular lumen, and loss of blood vessels, suggesting that interventions, which successfully ameliorated PH, would act by preventing or reversing such structural changes. The results of the present study cast doubt on this paradigm by demonstrating that chronic hypoxia did not cause a structurally based reduction of pulmonary vascular lumen diameter, nor did it cause a loss of pulmonary vessels. Moreover, we report that chronic inhibition of ROCK abrogated the development of hypoxic PH, not by preventing structural encroachment into the vascular lumen, but by inhibiting sustained pulmonary vasoconstriction. Importantly, we also found hypoxia-induced capillary angiogenesis in the adult lung that was dependent on the ...
R.J. Simpson, K. Raja, T.J. Peters; Studies of Iron Uptake by Duodenal Brush Boeder Membrane Vesicles Prepared Prom Normal and Hypoxic Mice. Clin Sci (Lond) 1 September 1983; 65 (3): 68P. doi: https://doi.org/10.1042/cs065068P. Download citation file:. ...
The effects of intravenous endothelin-1 (ET-1) on the ventilatory response to hypoxia were studied in healthy humans. Nine volunteers were each exposed twice to 4 hr eucapnic hypoxia. They received a continuous infusion of ET-1 during the ET-1 protocol and an infusion of saline during the control protocol. Plasma ET-1 levels and an index of ventilation were measured regularly. Hypoxia caused a rise in plasma ET-1 in the control protocol. Hypoxia also caused the index of ventilation to increase in both protocols, and this increase was greater in the ET-1 protocol than in the control protocol. These results are consistent with the hypothesis that ET-1 plays a role in controlling the ventilatory response to hypoxia in man.
Cerebral ischemia /hypoxia information including symptoms, causes, diseases, symptoms, treatments, and other medical and health issues.
Results Pre-incubation with rHDL inhibited the hypoxia-induced increases in PHD2 and PHD3 levels (32% and 45% respectively, p,0.05) while Siah1 and Siah2 mRNA levels were increased (58% and 88% respectively, p,0.05) with rHDL pre-incubation. Following siRNA knockdown of Siah1 and Siah2, HDL lost its ability to induce the expression of HIF-1α (11% reduction, p,0.05) and VEGF (18% reduction, p,0.05). Augmentation of tubulogenesis by HDL was attenuated in Siah siRNA-transfected cells (55% in siSiah1; 40% in siSiah2, p,0.05). Siah knockdown also abrogated HDL inhibition of hypoxia-mediated induction of PHD2 and PHD3 (p,0.05). PI3K and Akt are upstream regulators of HIF-1α/VEGF and also regulate Siahs. Specific inhibition of the PI3K/Akt pathway revealed that it plays a key role in HDL-induced elevations in Siah1 and Siah2 (37% and 20% reduction respectively, p,0.05) as well as HIF-1α and VEGF (65% and 15% reduction respectively, p,0.05). ...