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)

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

In the present study, respiratory drives to chemical stimuli and peripheral chemosensitivity were evaluated in patients with obstructive sleep apnoea (OSAS). The effects of oral administration of domperidone, a selective dopamine D2-receptor antagonist, were also examined, to study the respiratory effects of endogenous dopamine on peripheral chemoreceptors. Sixteen patients with OSAS and nine normal control subjects were studied. Respiratory responses to hypercapnia and hypoxia were measured using the rebreathing method and isocapnic progressive hypoxia method, respectively. The hypoxic withdrawal test, which measures the decrease in ventilation caused by two breaths of 100% O2 under mild hypercapnic hypoxic conditions (end-tidal oxygen and carbon dioxide tensions approximately 8.0 kPa and 5.3-6.7 kPa, respectively), was used to evaluate peripheral chemosensitivity. In the patients with OSAS, ventilatory responses to hypercapnia and hypoxia were significantly decreased compared with those of control subjects. Hypoxic withdrawal tests showed that peripheral chemosensitivity was significantly lower in patients with OSAS than in normal subjects. Hypercapnic ventilatory response and peripheral chemosensitivity were enhanced by administration of domperidone in the patients with OSAS, although no changes in either of these were observed in the control subjects. The hypoxic ventilatory response and peripheral chemosensitivity in the patients with OSAS were each significantly correlated with severity of hypoxia during sleep. These findings suggest that peripheral chemosensitivity in patients with obstructive sleep apnoea syndrome may be decreased as a result of abnormality in dopaminergic mechanisms and that the reduced chemosensitivity observed in patients with obstructive sleep apnoea syndrome may affect the severity of hypoxia during sleep.
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PMID:Depression of peripheral chemosensitivity by a dopaminergic mechanism in patients with obstructive sleep apnoea syndrome. 1006 91

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

Obstructive sleep apnoea syndrome (OSAS) is caused by obstruction or narrowing of the airway at various levels. The repair of one site only will not alleviate the syndrome if there are obstructions in other sites. Epiglottis prolapse during inspiration is an unusual cause of airway obstruction and a rare cause of OSA. Twelve cases of OSAS due to an abnormal epiglottis are presented. We present our approach to the diagnosis using fibre-optic examination of the hypopharynx, and our treatment using endoscopic carbon dioxide laser partial epiglottidectomy. We found in our series that in 11.5 per cent of patients who failed the uvulopalatopharyngoplasty procedure, the reason was a narrow airway at the hypopharyngeal level caused by an abnormal epiglottis. It is our suggestion that in these cases a laser partial epiglottidectomy should be performed. The results of this study show that partial epiglottidectomy can increase the cure rate of patients with obstructive sleep apnoea syndrome by 10-15 per cent.
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PMID:The epiglottis and obstructive sleep apnoea syndrome. 1021 Dec 16

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

Chronic heart failure (CHF) patients frequently show sleep-disordered breathing consisting of periodic breathing (PB) and Cheyne-Stokes respiration (CSR) with central sleep apnoea (CSA). Since the diagnosis of sleep-disordered breathing, in CHF patients, can be made only by means of full polysomnography, the aim of the present study was to evaluate whether or not daytime respiratory function can identify patients at risk of nocturnal PB and/or CSR/CSA. Twenty-seven patients (mean age 54 +/- 8.5 yrs), eight New York Heart Association Functional Class (NYHAFC) II, 17 NYHAFC III and two NYHAFC IV, with severe cardiac failure (cardiac output 2.0 +/- 0.66 L.min-1, ejection fraction 22.5 +/- 5.77%, pulmonary capillary wedge/pressure 23 +/- 9.05 mmHg). Mouth occlusion pressure (P0.1)/maximal inspiratory pressure (MIP) was significantly higher in patients with nocturnal CSR/CSA (5.04 +/- 1.49 versus 3.24 +/- 2.13%, analysis of variance (ANOVA) 0.03), whereas their arterial carbon dioxide tension (Pa,CO2) was significantly lower (4.15 +/- 0.56 (31.2 +/- 4.23 mmHg) versus 4.67 +/- 0.53 kPa (35.1 +/- 4 mmHg), ANOVA 0.02). Logistic regression analysis demonstrated that CSR/CSA occurrence may be predicted by daytime measurement of P0.1/MIP and Pa,CO2 (p = 0.04 and 0.01 respectively; odds ratio 1.93 and 0.76 respectively). The sensitivity was 70%, specificity 76.5%, false positive rate 36.4%, false negative rate 18.8%, positive predictive value 71.4% and negative predictive value 85%. This model seems useful for predicting respiratory pattern changes in chronic heart failure patients and the authors suggest that polysomnography be performed only in high-risk patients, saving costs and the resources of sleep laboratories.
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PMID:Identification of chronic heart failure patients at risk of Cheyne-Stokes respiration. 1054 73

Snoring, a leading symptom of the sleep apnoea syndrome (SAS), has been reported to be one of the risk factors for sleep-related cerebral strokes. Episodes of apnoea are accompanied by hypoxaemia as well as hypercapnia. As CO2 constitute a major regulatory factor controlling cerebral blood flow, it is likely that changes in cerebral perfusion are to be found in patients with SAS, which may be related to nocturnal stroke. A computer-assisted pulsed (2 mHz) Doppler ultrasonography system has been modified for continuous long-term and on-line recording of cerebral haemodynamics together with simultaneous polysomnography, continuous blood pressure recordings, and measurement of the end-expiratory CO2. The dynamics of cerebral blood flow velocity (CBFV) during sleep were measured in the right middle cerebral artery in 10 SAS patients. CBFV showed a characteristic nocturnal pattern with decreases during non-rapid eye movement (NREM) sleep and increases during REM sleep. Changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in CBFV. Dramatic increases in CBFV could be observed during apnoeic episodes, with maximum increases during REM sleep. CO2 reactivity and changes in CBFV related to apnoea duration were markedly increased during sleep compared with the waking state in SAS patients. The dynamic feature of CBFV in relation to sleep patterns reflects quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep in SAS patients as has been previously reported for normal subjects (Hajak et al. 1994). It supports a dissociation in the activity of central regulatory mechanisms during human sleep which might cause abnormal cerebral perfusion under certain circumstances. The increased CO2 reactivity during sleep in SAS suggests a 'hypersensitivity' of intracranial vasoactive receptors and/or disturbances in the central autonomic control of cerebrovascular functions. It may be concluded that, under certain conditions, the interaction of decreased cerebral perfusion in SAS patients with sleep-related cerebral perfusion patterns and haemodynamic changes during apnoeic episodes might lead to a critical reduction in cerebral perfusion.
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PMID:Cerebral perfusion during sleep-disordered breathing. 1060 90


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