Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objectives of the present study were to assess the level of exhaled breath markers indicating airway inflammation and oxidative stress in patients with obstructive sleep apnoea syndrome (OSAS) in comparison with non-apnoeic (obese and non-obese) subjects and investigate whether therapy with continuous positive airway pressure (CPAP) can modify them. The design was a retrospective observational study, set in Evgeneidio Hospital. Twenty-six OSAS patients and nine obese and 10 non-obese non-apnoeic subjects participated in this study. We measured nasal nitric oxide (nNO), exhaled nitric oxide (eNO), exhaled carbon monoxide (eCO) in exhaled breath, and 8-isoprostane, leukotriene B(4) (LTB(4)), nitrates, hydrogen peroxide (H(2)O(2)), and pH in exhaled breath condensate (EBC) before and after 1 month of CPAP therapy. The levels of eNO and eCO were higher in OSAS patients than in control subjects (p < 0.05). Nasal NO was higher in OSAS patients than in obese controls (p < 0.01). The level of H(2)O(2), 8-isoprostane, LTB(4), and nitrates were elevated in OSAS patients in comparison with obese subjects (p < 0.01). Conversely, pH was lower in OSAS patients than in non-apnoeic controls (p < 0.01). One month of CPAP therapy increased pH (p < 0.05) and reduced eNO (p < 0.001) and nNO (p < 0.05). Apnea/hypopnoea index was positively correlated with 8-isoprostane (r = 0.42; p < 0.05), LTB(4) (r = 0.35; p < 0.05), nitrates (r = 0.54; p < 0.001), and H(2)O(2) (r = 0.42; p < 0.05). Airway inflammation and oxidative stress are present in the airway of OSAS patients in contrast to non-apnoeic subjects. Exhaled breath markers are positively correlated with the severity of OSAS. One-month administration of CPAP improved airway inflammation and oxidative stress.
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PMID:Exhaled breath markers in patients with obstructive sleep apnoea. 1807 62

Intermittent hypoxia (IH) is thought to be responsible for many of the long-term cardiovascular consequences associated with obstructive sleep apnoea (OSA). Experimental human models of IH can aid in investigating the pathophysiology of these cardiovascular complications. The purpose of this study was to determine the effects of IH on the cardiovascular and cerebrovascular response to acute hypoxia and hypercapnia in an experimental human model that simulates the hypoxaemia experienced by OSA patients. We exposed 10 healthy, male subjects to IH for 4 consecutive days. The IH profile involved 2 min of hypoxia (nadir = 45.0 mmHg) alternating with 2 min of normoxia (peak = 88.0 mmHg) for 6 h. The cerebral blood flow response and the pressor responses to hypoxia and hypercapnia were assessed after 2 days of sham exposure, after each day of IH, and 4 days following the discontinuation of IH. Nitric oxide derivatives were measured at baseline and following the last exposure to IH. After 4 days of IH, mean arterial pressure increased by 4 mmHg (P < 0.01), nitric oxide derivatives were reduced by 55% (P < 0.05), the pressor response to acute hypoxia increased (P < 0.01), and the cerebral vascular resistance response to hypoxia increased (P < 0.01). IH alters blood pressure and cerebrovascular regulation, which is likely to contribute to the pathogenesis of cardiovascular and cerebrovascular disease in patients with OSA.
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PMID:Cardiovascular and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia in healthy humans. 1991 13

Endoscopic evaluation of the upper airway in patients with sleep disordered breathing (SDB) using rigid and flexible endoscopes is a typical investigation in otorhinolaryngology. Visualizing the anatomic structure as well as the dynamic mechanism of snoring and pharyngeal obstruction during wakefulness, natural sleep, and under sedation are of special interest. The results obtained have increased our understanding of SDB with obstruction of the upper airway. Videoendoscopy under sedation (ViSe) has become increasingly established as a tool to identify the therapeutic concept in cases of CPAP failure, leading to changes compared to the concept derived from basic awake endoscopy. The success of mandibular advancement devices can be adequately predicted. However, it remains unclear to what extent the success rate of surgery can be improved by ViSe. Further research into these approaches is needed in order to become valuable tools in the diagnostic work-up of patients with sleep apnea.
HNO 2010 Apr
PMID:[Endoscopy in sleep medicine]. 2033 65

Fatigue is a common problem in patients suffering from multiple sclerosis (MS). The presented case demonstrated concomitant severe central sleep apnea. Selection of the optimal ventilation modus was complex but proved successful. Given that daytime sleepiness is a frequent symptom in MS patients and that effective treatment options are available, sleep apnea should be considered and further classified by polysomnography in order to improve patients' quality of life.
HNO 2010 Apr
PMID:[Central sleep apnea in multiple sclerosis]. 2033 72

Chronic intermittent hypoxia (CIH) is a concomitant of sleep apnea that produces a slowly developing chemosensory-dependent blood pressure elevation ascribed in part to NMDA receptor-dependent plasticity and reduced nitric oxide (NO) signaling in the carotid body. The hypothalamic paraventricular nucleus (PVN) is responsive to hypoxic stress and also contains neurons that express NMDA receptors and neuronal nitric oxide synthase (nNOS). We tested the hypothesis that extended (35 d) CIH results in a decrease in the surface/synaptic availability of the essential NMDA NR1 subunit in nNOS-containing neurons and NMDA-induced NO production in the PVN of mice. As compared with controls, the 35 d CIH-exposed mice showed a significant increase in blood pressure and an increased density of NR1 immunogold particles located in the cytoplasm of nNOS-containing dendrites. Neither of these between-group differences was seen after 14 d, even though there was already a reduction in the NR1 plasmalemmal density at this time point. Patch-clamp recording of PVN neurons in slices showed a significant reduction in NMDA currents after either 14 or 35 d exposure to CIH compared with sham controls. In contrast, NO production, as measured by the NO-sensitive fluorescent dye 4-amino-5-methylamino-2',7'-difluorofluorescein, was suppressed only in the 35 d CIH group. We conclude that CIH produces a reduction in the surface/synaptic targeting of NR1 in nNOS neurons and decreases NMDA receptor-mediated currents in the PVN before the emergence of hypertension, the development of which may be enabled by suppression of NO signaling in this brain region.
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PMID:Chronic intermittent hypoxia induces NMDA receptor-dependent plasticity and suppresses nitric oxide signaling in the mouse hypothalamic paraventricular nucleus. 2082 73

Multilevel anatomic obstruction is often present in snoring and obstructive sleep apnoea (OSA). As the nose is the first anatomical boundary of the upper airway, nasal obstruction may contribute to sleep-disordered breathing (SDB). A number of pathophysiological mechanisms can potentially explain the role of nasal pathology in SDB. These include the Starling resistor model, the unstable oral airway, the nasal ventilatory reflex and the role of nitric oxide (NO). Clinically, a number of case-control studies have shown that nasal obstruction is associated with snoring and mild SDB. However, there is not a linear correlation between the degree of nasal obstruction and the severity of SDB, while nasal obstruction is not the main contributing factor in the majority of patients with moderate to severe OSA. Randomised controlled studies have shown that in patients with allergic rhinitis or non-allergic rhinitis and sleep disturbance, nasal steroids could improve the subjective quality of sleep, and may be useful for patients with mild OSA, however, they are not by themselves an adequate treatment for most OSA patients. Similarly, nasal surgery may improve quality of life and snoring in a subgroup of patients with mild SDB and septal deviation, but it is not an effective treatment for OSA as such. On the other hand, in patients who do not tolerate continuous positive airway pressure (CPAP) well, if upper airway evaluation demonstrates an obstructive nasal passage, nasal airway surgery can improve CPAP compliance and adherence.
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PMID:The role of the nose in snoring and obstructive sleep apnoea: an update. 2134 May 61

The obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is a common disorder, affecting around 2-4% of the middle-aged population. There is a strong association between OSAHS and hypertension, based on animal, large epidemiological and interventional studies. The epidemiological studies have shown a dose-response relationship between apnoea/hypopnoea index (AHI) and the risk of developing hypertension. Different mechanisms may have a role in the process of elevated blood pressure in OSAHS. Sympathetic activity is increased in OSAHS patients during sleep and wakefulness. This increase in sympathetic activity is probably due to activation of baroreflexes and chemoreflexes by frequent arousals and hypoxaemia a result of apnoea or hypopnoea events. Continuous positive airway pressure (CPAP) has been shown to reduce sympathetic stimulation and blood pressure in OSAHS patients. Altered endothelial function may also have a role in the pathogenesis of hypertension in OSAHS subjects. Reduction of nitric oxide (NO) production and increase in the formation of free radicals may be responsible for the impairment of the vasodilatation of micro-vasculature in these subjects as a result of hypoxaemia. It has been shown that effective CPAP therapy has a reversible effect on endothelial dysfunction.
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PMID:Obstructive sleep apnoea/hypopnoea syndrome and hypertension. 2174 71

Intermittent hypoxia (IH) resulting from sleep apnea can lead to pulmonary hypertension. IH causes oxidative stress that may limit bioavailability of the endothelium-derived vasodilator nitric oxide (NO) and thus contribute to this hypertensive response. We therefore hypothesized that increased vascular superoxide anion (O(2)(-)) generation reduces NO-dependent pulmonary vasodilation following IH. To test this hypothesis, we examined effects of the O(2)(-) scavenger tiron on vasodilatory responses to the endothelium-dependent vasodilator ionomycin and the NO donor S-nitroso-N-acetylpenicillamine in isolated lungs from hypocapnic-IH (H-IH; 3 min cycles of 5% O(2)/air flush, 7 h/day, 4 wk), eucapnic-IH (E-IH; cycles of 5% O(2), 5% CO(2)/air flush), and sham-treated (air/air cycled) rats. Next, we assessed effects of endogenous O(2)(-) on NO- and cGMP-dependent vasoreactivity and measured O(2)(-) levels using the fluorescent indicator dihydroethidium (DHE) in isolated, endothelium-disrupted small pulmonary arteries from each group. Both E-IH and H-IH augmented NO-dependent vasodilation; however, enhanced vascular smooth muscle (VSM) reactivity to NO following H-IH was masked by an effect of endogenous O(2)(-). Furthermore, H-IH and E-IH similarly increased VSM sensitivity to cGMP, but this response was independent of either O(2)(-) generation or altered arterial protein kinase G expression. Finally, both H-IH and E-IH increased arterial O(2)(-) levels, although this response was more pronounced following H-IH, and H-IH exposure resulted in greater protein tyrosine nitration indicative of increased NO scavenging by O(2)(-). We conclude that IH increases pulmonary VSM sensitivity to NO and cGMP. Furthermore, endogenous O(2)(-) limits NO-dependent vasodilation following H-IH through an apparent reduction in bioavailable NO.
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PMID:Intermittent hypoxia augments pulmonary vascular smooth muscle reactivity to NO: regulation by reactive oxygen species. 2175 77

Corticosteroids constitute an ideal treatment for various inflammatory and autoimmune disorders due to their anti-inflammatory and immunomodulatory actions. However, corticosteroids have a considerable number of side effects, including hypertension, diabetes, lipid disorders, sleep apnea, osteoporosis, myopathy, and disorders of coagulation and fibrinolysis, which are components of Cushing's syndrome (CS). Corticosteroid-induced side effects are dependent on the formulation, route, dose, and time of exposure. However, the underlying pathogenetic mechanisms have not been clearly defined. A large body of evidence supports the role of an imbalance between vasoconstriction and vasodilation with possible links to nitric oxide, prostanoids, angiotensin II, arginine vasopressin, endothelins, catecholamines, neuropeptide Y, and atrial natriuretic peptide. Increased oxidative stress, renin-angiotensin system activation, increased pressor response, metabolic syndrome, and sleep apnea appear to be pathogenetically involved as well. The ideal treatment is the withdrawal of corticosteroids, which is most often impossible due to the exacerbation of the underlying disease. Alternatively, a careful plan, including the proper selection of the formulation, time, and route, should be made, and each side effect should be treated properly. The focus of the research should be to develop synthetic corticosteroids with anti-inflammatory effects but fewer metabolic effects, which so far has been unsuccessful.
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PMID:Hypertension and other morbidities with Cushing's syndrome associated with corticosteroids: a review. 2194 34

Respiratory disorders are common and important complications in acromegaly. The prevalence of sleep apnea syndrome (SAS) in this group of patients is high (20%-50%). Consequences of SAS are serious and associated with increased morbidity and mortality, mainly as a result of cardiovascular complications. The symptoms of sleep apnea are often reversible with treatment. We report on an acromegaly patient presenting with excessive snoring and severe headaches caused by sleep apnea.
HNO 2012 Feb
PMID:[Rare differential diagnosis in a 40-year old patient with sleep apnea syndrome]. 2233 Oct 86


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