Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Weight loss reduces many of the health hazards associated with obesity including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, sleep apnea, hypoxemia and hypercarbia, and osteoarthritis. Potential adverse effects of weight loss include a greater risk for gallstone formation and cholecystitis, excessive loss of lean body mass, water and electrolyte problems, mild liver dysfunction, and elevated uric acid levels. Less consequential problems such as diarrhea, constipation, hair loss, and cold intolerance may also occur. The short-term adverse effects are not severe enough to contraindicate weight loss, nor do they outweigh its short-term benefits.
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PMID:Short-term medical benefits and adverse effects of weight loss. 836 5

To determine whether moderately obese, normocapnic, sleep apnea patients are distinguished from normal obese individuals by differences in waking pulmonary function and respiratory chemosensitivity, we compared the waking pulmonary function, hypercapnic, and hypoxic ventilatory responses of 35 nonhypercapnic sleep apnea patients (32 men and 3 women) with those of 17 age-, sex-, weight-, and obesity-matched nonapneic control subjects (16 men and 1 woman). The waking ventilatory response to hypercapnia was lower among sleep apnea patients (mean +/- SD, 2.05 +/- 1.29 L/min/mm Hg) than control subjects (3.02 +/- 2.05 L/min/mm Hg, p < 0.05). Patients with sleep apnea demonstrated a higher waking PaCO2 (40.4 +/- 2.9 vs 37.0 +/- 2.7 mm Hg, p < 0.001), and a lower waking PaO2 (81.4 +/- 11.7 vs 89.7 +/- 10.4 mm Hg, p < 0.03). The waking hypoxic ventilatory response, however, was not significantly different between the groups. Moreover, control subjects had a higher total lung capacity than sleep apnea patients (6.99 +/- 1.12 L and 6.27 +/- 1.09 L, respectively, p < 0.05). The lower hypercapnic ventilatory response, higher waking PaCO2, and lower total lung capacity in the sleep apnea patients resemble the pattern observed in patients with pickwickian syndrome. This suggests that disturbances in pulmonary function and ventilatory control in moderately obese sleep apnea patients are intermediate along a continuum from normal obesity to the pickwickian syndrome.
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PMID:Pulmonary function and respiratory chemosensitivity in moderately obese patients with sleep apnea. 803 13

The objective of our study was to assess the application of nasal continuous positive airway pressure (nCPAP) with supplemental oxygen for correction of upper airway obstructive episodes and hypoxaemia during sleep in stable patients with sleep apnoea-hypopnoea syndrome (SAHS) and severe chronic obstructive pulmonary disease (COPD). Ten male patients with symptomatic SAHS and severe COPD (forced expiratory volume in one second < 50% of predicted) were studied for three consecutive nights. Diagnostic polysomnography was performed the first night and repeated with increasing nCPAP levels, with and without supplemental oxygen on the second and third nights, respectively. Diagnostic polysomnography showed: mean (SD) apnoea-hypopnoea index 41 (22) events.h-1; mean arterial oxygen saturation (Sa,O2) was 86 (2)% and mean desaturation nadir was 81 (4)% during non-rapid eye movement (nREM) sleep and 80 (7)% and 73 (9)%, respectively during REM sleep. The application of nCPAP during the second night corrected apnoeas and hypopnoeas, but mean Sa,O2 remained < 90% in all patients. With the addition of oxygen at a flow of 1.5 L.min-1 at suboptimal nCPAP levels, we observed an increase in apnoea frequency, persistence of apnoeas at nCPAP levels which eliminated them when no supplemental oxygen was administered, and longer duration of apnoeas and hypopnoeas. However, when the effective nCPAP level of the second night was reached with supplemental oxygen during the third night, its efficacy in eliminating apnoeas and hypopnoeas was maintained and, furthermore, all patients presented Sa,O2 > 90%, with no greater hypercapnia cardiac arrhythmias. We conclude that nasal continuous positive airway pressure with supplemental oxygen constitutes a practical therapeutic alternative for hypoxic patients with sleep apnoea-hypopnoea syndrome and chronic obstructive pulmonary disease.
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PMID:Nasal continuous positive airway pressure with supplemental oxygen in coexistent sleep apnoea-hypopnoea syndrome and severe chronic obstructive pulmonary disease. 883 43

The clinical course and changes in hypercapnic ventilatory drive over time were serially assessed before and after tracheostomy placement in a 14 year old, morbidly obese female patient with Prader-Willi syndrome, severe obstructive sleep apnoea, and obesity-hypoventilation syndrome. A tracheostomy became necessary after supplemental oxygen and continuous positive airway pressure (CPAP) had failed to improve the severity of nocturnal hypoventilation. Continued improvement in the slope to rebreathing hyperoxic hypercapnia occurred from 2-10 weeks after tracheotomy in conjunction with night-time bilevel pressure ventilation, and remained unchanged thereafter. In contrast, increases in mean resting minute ventilation at an end-tidal carbon dioxide tension (PET,CO2) of 8 kPa (60 mmHg) were documented even after 30 weeks. This case study illustrates the time-frame of dynamic ventilatory changes occurring after removal of upper airway resistance and normalization of nocturnal alveolar ventilation.
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PMID:Longitudinal assessment of hypercapnic ventilatory drive after tracheotomy in a patient with the Prader-Willi syndrome. 883 75

The static charge sensitive bed (SCSB) is a simple and noninvasive device used for the detection of sleep apnoea. In addition to episodes of apnoea or hypopnoea, heavy snorers commonly present with episodes of high frequency spiking on the SCSB. These spiking episodes have been claimed to represent partial upper airway obstruction during sleep, but the mechanism of their appearance is not known. We studied the SCSB spiking phenomenon in awake subjects during experimental respiratory challenge. One female and five male volunteers were studied whilst breathing freely, during hypoxia, hypercapnia and inspiratory and expiratory loading. Oxygen saturation, end-tidal carbon dioxide tension, minute ventilation, oesophageal pressure, electrocardiographic activity (ECG), blood pressure and the SCSB signals were monitored. During free breathing, the SCSB high frequency signal consisted of low amplitude complexes with close time relationship to the cardiac cycle. During respiratory challenge, spiking occurred. These spikes showed no time relationship to the cardiac cycle, but were time-linked to the onset of inspiration or expiration. Spike amplitude correlated with breathing frequency (r2 = 0.59; p < 0.005) and variation in oesophageal pressure (r2 = 0.57; p < 0.005). We conclude that during quiet, unobstructed breathing the static charge sensitive bed high frequency signal represents cardiac activity (ballistocardiogram), whereas during high-drive breathing high frequency spikes are produced. These spikes are respiratory in origin and are likely to represent fast components of respiratory movements. Our results support the use of static charge sensitive bed spiking as a noninvasive measure of breathing stimulation.
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PMID:Respiratory challenge induces high frequency spiking on the static charge sensitive bed (SCSB). 888 95

This project examined the effects of alterations in respiratory drive on the occurrence of sleep apnea in Northern elephant seal pups (Mirounga angustirostris). Sleep pattern was unaffected by levels of hypoxia (approximately 13%) or hypercapnia (approximately 6%) that doubled respiratory frequency during slow-wave sleep (SWS). During sleep in air, short periods of continuous breathing (mean length = approximately 2.6 min) alternated with periods of apnea (mean length = approximately 6.1 min). Under hypoxic or hypercapnic conditions, the frequency of occurrence of apneas was reduced primarily due to the occurrence of some sleep episodes without periods of apnea. In episodes in which apneas did occur, they began later in the sleep episodes, but their length and the length of the periods of eupnea were not significantly altered. During each period of eupnea, however, the instantaneous respiratory rate and the total number of breaths increased. Breathing during sleep was restricted to SWS, never occurring during rapid eye movement (REM) sleep, regardless of the respired gas mixture. If the levels of hypoxia and hypercapnia were raised further, all episodes of apnea during sleep could be eliminated together with all episodes of REM sleep. One interpretation of the data is that the threshold for altering breathing during eupnea (instantaneous breathing frequency and number of breaths per episode of eupnea) is lower than that for altering the lengths of the periods of apnea and eupnea and that the muscle atonia associated with REM sleep extends to all respiratory muscles.
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PMID:Effects of hypoxia and hypercapnia on patterns of sleep-associated apnea in elephant seal pups. 889 95

We report 2 patients with multiple sclerosis (MS) who were symptomatic but ambulatory, and died in their sleep. Sleep studies in 1 patient showed hypercarbia and hypoxia accompanying sleep. In both cases autopsy showed plaques of multiple sclerosis in the medulla oblongata, incompletely involving the neuroanatomic areas of the medullary reticular formation controlling automatic breathing. A systematic analysis of the location of the plaques in relation to areas known to be important in breathing control revealed that the regions corresponding to the ventral nuclear complex of respiratory control in animals were incompletely and unilaterally involved in both cases. Close correlation with nuclei that have been demonstrated in animal experiments to be important in descending respiratory control of phrenic and intercostal musculature was not possible due to possible differences in anatomy between animals and humans, and the fact that plaques of MS affect axons of passage and spare neuronal cell bodies. Nevertheless, the cases clearly illustrate that patchy, unilateral lesions of the medullary reticular formation in humans can give rise to sleep disordered breathing. The cases also illustrate the risk of death during sleep in MS patients with demyelination in the medulla oblongata, and demonstrate the need to carefully examine the medulla in MS patients if they die unexpectedly during sleep.
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PMID:Multiple sclerosis with medullary plaques and fatal sleep apnea (Ondine's curse). 892 93

An 18-year-old, previously healthy male presented with bilateral pneumonia and acute respiratory failure with severe carbon dioxide retention. The presence of mild brainstem signs and hypoventilation led to the discovery of a platybasia, basilar invagination, and kinking of the medulla oblongata with early syrinx. He was operated upon but postoperatively was noted to have a mixed type of sleep apnea. This case illustrates the diagnostic challenge in acute respiratory failure in a previously healthy young person and the possible pathogenic mechanisms underlying it.
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PMID:A cranio-cervical malformation presenting as acute respiratory failure. 893 17

Acute intermittent repetitive hypoxia simulating sleep apnoea syndrome is responsible for acute rises in blood pressure (BP). In the rat, the BP rises are enhanced by added hypercapnia. To investigate the role of the autonomic nervous system (ANS) in acute hypertension during repetitive hypoxia alone, FiO2 (inspiratory fractional concentration of oxygen) 2 to 5%, or combined with hypercapnia FiCO2 (inspiratory fractional concentration of carbon dioxide) 2 to 5%, we used autonomic blockade by atropine (1 mg kg-1) + propranolol (1 mg kg-1)-phentolamine (1 mg kg-1). Seven Wistar male rats were chronically instrumented with two aortic and venous catheters. Repetitive administration of N2 and N2 + CO2 for 10s followed by 20s compressed air was repeated for 4-5 min before (control) and after autonomic blockade. After autonomic blockade there was no significant difference in mean blood pressure (MBP) during severe hypoxia (SHO) (14.9 +/- 0.5 mmHg) compared to control (10.5 +/- 0.9 mmHg), while MBP was significantly decreased in severe hypoxia + hypercapnia (SHOHC) (14.1 +/- 0.4 mmHg) compared to control (26.8 +/- 0.3 mmHg) (p < 0.001). We conclude that the acute BP rise observed during hypoxic breathing is not due to the activation of ANS, but when hypercapnia is added to the hypoxic stimulus about half of pressor response is caused by ANS.
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PMID:Role of the autonomic nervous system in the acute blood pressure elevation during repetitive hypoxic and hypercapnic breathing in rats. 897 56

A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
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PMID:Central sleep apnea. 904 68


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