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)

Sleep apnoea is common in patients with heart failure. While most patients have central sleep apnoea (CSA), a minority have obstructive sleep apnoea (OSA). The pathophysiology of CSA is not well understood. We hypothesized that central chemosensitivity would be an important pathophysiological factor in patients with CSA, and not in OSA. The aim of this study was to compare ventilatory responses between patients with CSA and those with OSA. Acute ventilatory responses to eucapnic hypoxia and hyperoxic hypercapnia were measured during wakefulness in 34 patients (33 males and one female, aged 59+/-8 yrs (mean+/-SD)), with stable medically-treated left ventricular dysfunction (LVD) and sleep apnoea (18 OSA and 16 CSA). Patients with CSA had a decreased awake end-tidal carbon dioxide tension (4.1+/-0.5 kPa), increased ventilatory response to carbon dioxide (0.65+/-0.43 L.min.(-1).kPa PCO2(-1)), and eucapnic hypoxic responses in the normal range (0.6+/-0.4 L.min(-1)/% fall in arterial oxygen saturation (Sa,O2)). In contrast, patients with OSA had normal end-tidal carbon dioxide tension (4.9+/-0.5 kPa), and normal ventilatory responses to hypercapnia (0.29+/-0.16 L.min(-1).kPa PCO2(-1)) and hypoxia (0.5+/-0.5 L-min(-1)/% fall in Sa,O2). These findings suggest that augmented chemosensitivity to hypercapnia may be an important factor in the pathophysiology of central sleep apnoea in patients with heart failure.
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PMID:Ventilatory control in patients with sleep apnoea and left ventricular dysfunction: comparison of obstructive and central sleep apnoea. 954 61

Recent results in animals have suggested that repetition of hypoxaemic stimuli may result in a progressive increase in pulmonary arterial pressure (Ppa). The purpose of the present study was to investigate the effects of recurrent obstructive apnoeas on Ppa. We have, therefore, examined the nocturnal trend of Ppa in seven obstructive sleep apnoea syndrome (OSAS) patients and in five snorers. Mean Ppa was measured before, at the start, at the end and after the selected apnoeas. The analysis was performed for each 1 h period for at least 7 h throughout the night on at least 10 randomly selected apnoeas per hour. In snorers, 100 randomly chosen values were measured during every hour of the night. In the morning after the nocturnal study, the Ppa responses to acute hypoxia and hypercapnia were measured. No Ppa changes throughout the 7 h were found during sleep in snorers [Ppa slope:-0.002+/-0.10 mmHg x h(-1)]. In OSAS patients a small but significant increase in Ppa throughout the night was noted, affecting the values before [Ppa slope: 0.7+/-0.16 mmHg x h(-1)], at the start of apnoea [Ppa slope: 0.530.1 mmHg x h(-1)] as well as at the end [Ppa slope: 0.44+/-0.08 mmHg x h(-1)] and in the postapnoeic period [Ppa slope: 0.55+/-0.1 mmHg x h(-1)]. When we limited the analysis to nonrapid eye movement (NREM) sleep, a trend in progressive Ppa was also present, irrespective of changes in apnoea duration and apnoea desaturation. The Ppa rise during the night was not affected by diurnal Ppa pulmonary vascular response to hypoxia and hypercapnia or indices of sleep apnoea severity. We conclude that in obstructive sleep apnoea, pulmonary artery pressure progressively increases during the night, reflecting the cumulative effects of apnoeas and nocturnal hypoxaemia.
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PMID:Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas. 955 51

We evaluated the effect of non-invasive nocturnal ventilation with the bi-level positive airway pressure (BiPAP) ventilator in 12 overweight patients with verified obstructive sleep apnoea syndrome (OSAS) and nocturnal hypercapnia. All patients exhibited subsequently less overnight CO2 accumulation (p < 0.0001), the desaturation event frequency was reduced (p < 0.002), daytime O2 tension rose (p < 0.001), daytime CO2 tension was reduced (p < 0.01), and apnoeas were eliminated. All symptoms characterising the syndrome, when present at the beginning of the therapy, were eliminated during the treatment. Patient compliance was high. This study showed that OSAS patients with hypercapnia can be effectively treated by BiPAP ventilation during sleep.
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PMID:Bi-level positive airway pressure treatment of obstructive sleep apnoea syndrome. 958 Sep 22

We present the case of a young adult with type I Arnold-Chiari malformation (AMC1) and syringomyelia who developed central sleep apnoea and chronic respiratory failure, successfully treated with nocturnal noninvasive positive pressure ventilation ventilation (NIPPV). An extensive syringomyelic cavity (from bulbar to L4 segment) with severe impairment of the IX cranial nerve was documented and remains, although reduced, after the neurosurgical treatment. At baseline evaluation, the patient showed a moderate restrictive ventilatory defect, severe hypercapnic respiratory failure, abnormal control of breathing characterized by the absence of response to hypoxia and hypercapnia, and severe nocturnal central apnoeas. Nocturnal NIPPV was then started in the A/C mode with an improvement in blood gas values. Further evaluations were performed 10 and 18 months later. A progressive significant improvement of lung volumes, both in sitting and supine position, associated with a slight improvement of blood-gas values were observed. Nonetheless, the breathing pattern abnormalities persisted. Polysomnographic evaluation during mechanical ventilation showed a normalization of breathing pattern with arterial oxygen saturation (SaO2) > 90% throughout the night.
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PMID:Chronic respiratory failure in a patient with type I Arnold-Chiari malformation (ACM1) and syringomyelia. 968 98

Sleep-apnea syndrome is a serious problem in respiratory care. Considerable attention has been paid to it, because it sometimes produces severe hypoxia and hypercapnia, and can cause death. We present a case of a six-year-old girl who showed sleep-apnea syndrome. She suffered from bilateral paralysis of the diaphragm after cardiac surgery and had to be managed under mechanical ventilation for three months. When weaning was tried from mechanical ventilation, she frequently showed apnea lasting over 15 seconds at night, and she was diagnosed as having sleep apnea. She was medicated with theophylline to stimulate the so-called respiratory center. Next day she was successfully weaned from mechanical ventilation. After she had been weaned from mechanical ventilation, hypoxia, hypercapnia, and tachycardia were detected by respiratory monitor at night. The respiratory monitor enabled us to identify the clinical appearance of sleep-apnea, and theophylline may have contributed to its improvement.
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PMID:[A case of central sleep-apnea syndrome accompanied by bilateral paralysis of the diaphragma after pediatric cardiac surgery]. 969 91

The objective of this study was to investigate the effects of obstructive sleep apnoea on: (i) PaCO2 levels; (ii) coagulation systems (plasma fibrinogen levels and whole blood viscosity); and (iii) heat shock proteins (HSPs) levels, which are also called stress proteins, in patients with obstructive sleep apnoea syndrome (OSAS). Patients treated with or without nasal continuous positive airway pressure (NCPAP) had arterial blood gases, plasma fibrinogen, haematocrit, serum total protein and changes in PaCO2 (estimated by transcutaneous PaCO2) measured before and after polysomnography. Heat shock protein 72 levels in peripheral blood mononuclear cells were also measured during sleep with and without NCPAP. OSAS patients with hypercapnia demonstrated significant increases in PaCO2 in the morning compared with the previous night. In such OSAS patients, treatment with NCPAP resulted in a normalization of the 20 mg/dL increase in fibrinogen levels which had been seen previously in the morning after sleep. Basal HSP 72 levels (08.00 pm before sleep) were high in OSAS patients compared to normal subjects and progressively decreased during sleep in the absence of NCPAP therapy. NCPAP relieved disabling day-to-day symptoms in addition to improving cardiovascular morbidity in patients with OSAS. Therefore it is important to understand the effects of OSAS on various organ systems as the prevalence of patients with OSAS is high.
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PMID:New insights into the therapy and pathophysiology of patients with obstructive sleep apnoea syndrome. 969 24

A 21 yr old with deep breathing and awake apnoea, who had recurrent hypoxaemia and hypercapnia without sleep apnoea, was presented. Although the organic abnormality responsible for the breathing disturbance was not found, administration of acetazolamide facilitated several breaths between sighs, and the patient's hypoxaemia with hypercapnia improved. Some patients who have abnormalities in the cortical control of breathing that cannot be detected by present methods of examination may experience some improvement in breathing with the administration of chemical stimulants such as acetazolamide.
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PMID:Deep breathing and awake apnoea in a patient who had recurrent hypoxaemia and hypercapnia without sleep apnoea. 976 6

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.
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PMID:Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome. 984 56

The failure to eradicate group A beta-hemolytic streptococci from the pharynx is partly due to a low compliance, but above all, an alteration of the oropharyngeal microbiological flora: reduction of alpha-haemolytic streptococci which inhibit group A beta-hemolytic streptococci and increase of microorganisms such as Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis. These latter act indirectly destroying the beta-lactamic ring of penicillins. However, this obstacle is overcome by the use of antibiotics which do not contain beta-lactamic rings such as macrolides or associating amoxicillin with clavulanic acid or with new cephalosporins which are more resistant to beta lactamases. To restrict the diffusion of resistance to antibiotics, it is essential to limit their use diagnosing streptococcal tonsillopharyngitis more precisely, thanks to an improved use of micro-biological diagnostic tests and by a more extended use of tonsillectomy in recurrent tonsillitis (more than 6-7 in 1-2 years). Adenoiditis is closely related to the post nasal drip syndrome, to recurrent otitis media and to otitis media with effusion. All these situations could, therefore, represent an indication, although not well defined, for adenoidectomy. Nasopharyngeal obstruction due to adeno-tonsillar hypertrophy becomes critical during sleep when the hypotony of the upper airway muscles becomes additional to the anatomical obstruction. At this point the inspiratory effort required and the consequent decrease of intra airway pressure increase the pharyngeal obstruction suctioning the pharyngeal walls toward the median line. The resulting clinical picture is defined as sleep-disordered breathing (SDB) due to adenotonsillar hypertrophy (idiopathic), to be distinguished from SDB due to cranio-facial abnormalities or neuromuscular diseases. SDB includes both the more serious sleep apnea syndrome and the less severe upper airway respiratory resistance syndrome. A combination of symptoms and clinical data detectable both while awake or asleep, make the diagnosis simple. During sleep, both apnea and paradoxical inspiratory movements are highly specific while snoring is highly sensitive. To evaluate nasopharyngeal obstruction radiography and optic fibre endoscopy are both equally reliable. The gold standard test for non idiopathic SDB is the polysomnography, whereas for SDB, due to adenotonsillar hypertrophy, one is limited today to the recording during sleep of O2 saturation or of end tidal CO2. These investigations are, however, generally used up to 2 years of age, when the decision to carry out an adenoidectomy and especially a tonsillectomy is more difficult because of the greater risks which surgery involves at this age. The pharmacological therapy has a purely palliative function and is based on antibiotics, local vasoconstrictors, steroids and theophylline which acts more as an antiflogistic than as a breath stimulant. O2 therapy and nasal continuous positive airway pressure (CPAP) give better results, but are more difficult to carry out, in particular on a long term basis. Adenoidectomy especially if associated with tonsillectomy, leads to the resolution of the symptoms, but not always to a normalization of functional alterations (hypoxia and hypercapnia). For this reason, it is necessary to act on other factors which cause oedema of the nasopharyngeal mucosa contributing to the obstruction. In this area, the prevention of viral infections can be achieved by vaccination against influenza and by preventing the child from attending crowded day care centers. With regard to allergic inflammation, skin prick tests could be a first step in view of allergens avoidance measures. With regard to indoor air pollution, passive smoke must be stopped and the child kept out of the kitchen.
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PMID:[The tonsils and adenoids as a site of infection and the cause of obstruction]. 986 45

Acetazolamide, a carbonic anhydrase inhibitor, is used in patients with chronic obstructive pulmonary diseases and central sleep apnoea syndrome and in the prevention and treatment of the symptoms of acute mountain sickness. In these patients, the drug increases minute ventilation (V'E), resulting in an improvement in arterial oxygen saturation. However, the mechanism by which it stimulates ventilation is still under debate. Since hypoxaemia is a frequently observed phenomenon in these patients, the effect of 4 mg x kg(-1) acetazolamide (i.v.) on the ventilatory response to hypercapnia during hypoxaemia (arterial oxygen tension (Pa,O2)=6.8+/-0.8 kPa, mean+/-SD) was investigated in seven anaesthetized cats. The dynamic end-tidal forcing (DEF) technique was used, enabling the relative contributions of the peripheral and central chemoreflex loops to the ventilatory response to a step change in end-tidal carbon dioxide tension, (PET,CO2) to be separated. Acetazolamide reduced the CO2 sensitivities of the peripheral (Sp) and central (Sc) chemoreflex loops from 0.22+/-0.08 to 0.11+/-0.03 L x min(-1) x kPa(-1) (mean+/-SD) (p<0.01) and from 0.74+/-0.32 to 0.40+/-0.10 L x min(-1) x kPa(-1) (p<0.01), respectively. The apnoeic threshold B (x-intercept of the ventilatory CO2 response curve) decreased from 2.88+/-0.97 to 0.95+/-0.92 kPa (p<0.01). The net result was a stimulation of ventilation at PET,CO2 <5 kPa. The effect of acetazolamide is possibly due to a direct effect on the peripheral chemoreceptors as well as to an effect on the cerebral blood flow regulation. Possible clinical implications of these results are discussed.
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PMID:Effect of low-dose acetazolamide on the ventilatory CO2 response during hypoxia in the anaesthetized cat. 987 70


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