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)

Obstructive sleep apnoea syndrome (OSAS) is associated with systemic arterial hypertension and cardiac arrhythmias and may lead to cardiovascular complications. Dysfunction of the autonomic nervous system (ANS) may play a role in the development of cardiovascular complications. The aim of this work was to study the ANS by spectral analysis of the heart rate variability (HRV) at rest and after stress (head-up tilt test) in a group of normotensive awake OSAS subjects. We studied 22 males with OSAS, aged 47.6 +/- 13.1 yrs, with a body mass index (BMI) 35.6 +/- 7.7 kg.m-2 and blood systolic and diastolic pressure (BSP and BDP, respectively) of 128 +/- 16 and 80 +/- 9 mmHg. Nineteen healthy males were studied as controls. Autonomic investigations were performed using the computerized power spectral analysis of HRV with autoregressive modelling which identifies low frequency (LF), as a marker of sympathetic activity and high frequency (HF), as a marker of vagal activity. OSAS patients showed greater sympathetic activity (LF) at rest than normal subjects, and an abnormal response to the head-up tilt test compared to control subjects. Five OSAS patients behaved like control subjects. Comparison of the functional parameters between these five OSAS patients and the other 17 OSAS patients showed a statistically significant difference for only basal arterial carbon dioxide tension (Pa,CO2) and minimal nocturnal oxyhaemoglobin (HbO2) saturation (NADIR). Our study shows autonomic nervous system dysfunction in patients with obstructive sleep apnoea syndrome, which may have facilitated a pathophysiological link with the cardiovascular complications observed in these patients.
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PMID:Autonomic dysfunction in normotensive awake subjects with obstructive sleep apnoea syndrome. 963 3

One month administration of acetazolamide (ACET) (at sea level) improves periodic breathing and decreases the number of central apneas (CA) (De Backer et al., 1995 Am. J. Respir. Crit. Care Med. 151, 87-91) in nonhypercapnic central apnea syndrome. It remains unclear whether cessation of therapy would provoke recurrence of symptoms. In the present study we evaluated the number of CA after 1 and 6 months interruption of ACET therapy. Eight patients with central sleep apnea were included [central apnea index (CAI) > 5 or apnea and hypopnea index (AHI) > 10 and obstructive apnea index (OAI) < 5]. Polysomnography was repeated once after 1 month treatment (N2), after 1 month off treatment (N3) and after 6 months off treatment. CAI (25 +/- 10 at N1) decreased during N2 (4 +/- 2) and N3 (5 +/- 3) and remained low after N4 (3 +/- 1). However an increase in the number of obstructive apneas and central hypopneas could be observed together with a shift from central apnea to hypopnea after N4. Maybe ACET induces a long lasting resetting of the CO2 threshold which is still present after interruption of the therapy.
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PMID:Central sleep apnea after interrupting longterm acetazolamide therapy. 969 83

The operation of Laser Assisted Uvulopalatoplasty (LAUP) as described by Kamami is now becoming more commonly used in the treatment of snoring and obstructive sleep apnoea. The authors have treated 95 snoring patients, varying the lengths of the soft palate incisions and percentage of uvula excised. All operations were carried out under general anaesthesia using a CO2 laser. Pilot studies showed incisions that are 25% of the distance between the free edge of the soft palate to the hard palate junction and excision of 50% of the uvula give good results with minimal complications. A further study using these parameters was conducted and postoperative evaluation including polysomnography confirmed this procedure to be effective in reducing snoring levels both subjectively and objectively.
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PMID:Laser Assisted Uvulopalatoplasty: an objective evaluation of the technique and results. 976

The paper concerns surgical treatment of rhonchus. 41 patients with rhonchus and sleep apnea were examined and treated. The patients were characterized by obesity, short fat neck, diseases of the upper respiratory tracts (chronic tonsillitis, adenoids, distortion of the nasal septum, deformity of the external nose, weakness of the palatine curtain). After cleansing of the upper respiratory tracts and recovery of nasal breathing all the patients underwent CO2 laser surgery on the soft palate with good effect.
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PMID:[On aspects of surgical treatment of pathological snoring]. 979 29

Failure to autoresuscitate by hypoxic gasping during prolonged sleep apnea has been suggested to play a role in sudden infant death. Furthermore, maternal smoking has been repeatedly shown to be a risk factor for sudden infant death. The present experiments were carried out on newborn rat pups to investigate the influence of perinatal exposure to nicotine (the primary pharmacological and addictive agent in tobacco) on their time to last gasp during a single hypoxic exposure and on their ability to autoresuscitate during repeated exposure to hypoxia. Pregnant rats received either nicotine (6 mg. kg-1. 24 h-1) or vehicle continuously from day 6 of gestation to days 5 or 6 postpartum via an osmotic minipump. On days 5 or 6 postpartum, pups were exposed either to a single period of hypoxia (97% N2-3% CO2) and their time to last gasp was determined, or they were exposed repeatedly to hypoxia and their ability to autoresuscitate from primary apnea was determined. Perinatal exposure to nicotine did not alter the time to last gasp, but it did impair the ability of pups to autoresuscitate from primary apnea. After vehicle, the pups were able to autoresuscitate from 18 +/- 1 (SD) periods of hypoxia, whereas, after nicotine, the pups were able to autoresuscitate from only 12 +/- 2 periods (P < 0.001) of hypoxia. Thus our data provide evidence that perinatal exposure to nicotine impairs the ability of newborn rats to autoresuscitate from primary apnea during repeated exposure to hypoxia, such as may occur during episodes of prolonged sleep apnea.
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PMID:Perinatal nicotine exposure impairs ability of newborn rats to autoresuscitate from apnea during hypoxia. 984 27

Previously we showed that CO2 drive is increased in patients with obstructive sleep apnea (OSA). In the present study we would like to evaluate a possible relationship between CO2 drive and characteristics of apneas in obstructive and central sleep apnea (CSA). We compared the hypercapnic ventilatory response (HCVR) between patients with OSA and CSA. HCVR was correlated with total event time and mean event duration in both groups. 17 normocapnic patients in each group and 14 controls were studied. The apnea patients were matched for apnea-hypopnea index, age, sex, and BMI. SHCVR (slope) tended to be higher in apnea patients than in controls without statistical significancy: controls 1.65 (0.16), CSA 2.17 (0.22), OSA 2.55 (0.35) (l/min per mmHg) (P = 0.13). A significant correlation was found between HCVR and event time in CSA (0.52, P = 0.04) and between HCVR and apnea mean duration in OSA (r = 0.52, P = 0.04). We conclude that while CO2 drive was not statistically increased in both apnea types, small changes can contribute to breathing instability and may increase the total event time (in CSA) but may also shorten the apnea duration (in OSA).
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PMID:Relationship between CO2 drive and characteristics of apneas in obstructive and central sleep apnea. 986 92

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

Strained breathing is a natural respiratory pattern, with cardiovascular implications. It is associated with social factors, attention, expectation, and anxiety and with defense behavior in animals. An inhibition of active behavior is characteristic. Strained breathing is based on the functional heterogeneity of the medullary postinspiratory neurons. In stressful circumstances, muscle tension and laryngeal reflexes induce a strong reduction of airflow in the glottis, resulting in a prolonged Stage I of expiration and an elevated intrathoracic pressure. The resulting elevations of blood pressure and CO2 level further stimulate the strained breathing pattern. The straining factor intrathoracic pressure is an important psychophysiological parameter. Functional aspects of strained breathing may be an elevated brain perfusion and the prevention of hyperventilation. It induces blood pressure oscillations and respiratory sinus arrhythmia. Frequent strained breathing may contribute to cardiovascular pathology and sleep apnea, creating a link between functional behavior and disease.
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PMID:The psychobiology of strained breathing and its cardiovascular implications: a functional system review. 1019 63

The objective was to examine whether abnormal breathing during sleep may affect regulation of ventilation after awakening in patients with obstructive sleep apnoea (OSAS). In 19 patients with OSA and 12 normal subjects we examined ventilatory responses to hypoxia (HVR) and to hypercapnia (HCVR) before and after sleep (BS and AS), and compared the changes in ventilatory responses with respiratory events during sleep. In the OSA group, the values of resting ventilation were significantly smaller in AS than those in BS and end-tidal partial pressure of CO2 in arterial blood (Pco2) (PETCO2) rose significantly from BS to AS. The slopes of the HVR or HCVR did not differ between BS and AS. However, both the response lines shifted downward and minute ventilation (VE)80 (VE at arterial oxygen saturation (Sao2) of 80%) in HVR and VE60 (VE at PETCO2 of 60 mmHg) in HCVR decreased significantly from BS to AS. The percentage changes of VE80 and VE60 were significantly correlated with mean Sao2, total sleep time below Sao2 of 90% and lowest Sao2 during sleep. However, in normal subjects we observed no circadian variation in their ventilatory responses. These data support the hypothesis that repeated episodes of nocturnal hypoxia and hypercapnia may modify the regulation of ventilation after awakening in patients with OSA.
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PMID:Regulation of ventilation before and after sleep in patients with obstructive sleep apnoea. 1038 30


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