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)

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

The prevalence of sleep apnea syndrome (SAS) is approximately 7.5% in Japanese adults aged 18-68 years old. SAS is characterized by repeated episodes of apnea, especially obstructive apnea, during sleep. Severe SAS has life-threatening complications such as pulmonary hypertension, arrhythmias, right heart failure or brain damage, which could be caused by hypoxemia and/or hypercapnia. Upper airway relaxation is responsible for the obstruction during apnea, and an increase in the activities of the upper airway muscles dilates and stiffens the upper airway wall. Maintaining the activities of the upper airway muscles may contribute to keeping the airway patent. Submental electrical stimulation of the upper airway muscles would be a novel treatment method for obstructive apnea.
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PMID:New strategies of screening and treatment for sleep apnea syndrome. 1032 56

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

Impaired vasomotor reactivity of the cerebral vessels on morning awakening has been suggested as one of the mechanisms underlying the predisposition to stroke in the morning. This study investigated cerebrovascular reactivity to hypercapnia on morning awakening and its association with specific sleep-related parameters, including sleep-disordered breathing. Thirty patients undergoing nocturnal diagnostic polysomnography for sleep apnea underwent transcranial Doppler ultrasonography of the middle cerebral artery immediately before going to bed and immediately on morning awakening. Results indicated a morning reduction in cerebral blood flow velocity (CBFV) relative to values from the preceding evening both while breathing room air and 5% CO(2). Hypercapnia was associated with the expected increase in CBFV in both evening and morning. The evening-to-morning difference in CBFV during CO(2) inhalation was independently associated with both overnight CO(2) retention and number of movements with arousal per hour of sleep. Results indicated that more fragmented sleep and greater CO(2) retention during sleep predicted a diminished hypercapnic vasomotor response in the morning. Sleep fragmentation predicted approximately twice the variance in morning hypercapnic vasomotor reactivity relative to overnight CO(2) retention (24 versus 13%). No other polysomnographic measures predicted evening-to-morning differences in vasomotor reactivity. These results are consistent with a body of literature suggesting that sleep loss and sleep fragmentation are associated with blunted hypercapnic ventilatory response.
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PMID:Sleep fragmentation and morning cerebrovasomotor reactivity to hypercapnia. 1050 14

Multiple factors may be responsible for acute and chronic blood pressure changes during obstructive sleep apnoea. A popular hypothesis is that recurrent episodic hypoxia stimulates chemoreceptors which, in turn, cause sympathetically mediated vasoconstriction and perhaps long-term vascular remodelling. Disruption of sleep architecture secondary to frequent arousals may also cause chronic stress which may contribute to diurnal hypertension. A less likely factor elevating blood pressure is the effect of abrupt intra-thoracic pressure changes on venous return and cardiac output. The rat responds to chronic, recurrent episodic hypocapnic hypoxia (12-s bursts of nitrogen followed by air into Plexiglas chambers, every 30 s, 7 h d-1, 2-4% nadir ambient oxygen) with sustained increase in diurnal blood pressure 11-14 mmHg). Subsequent studies reveal that carotid sinus nerve section (chemodenervation) and chemically induced peripheral sympathetic denervation with the neurotoxin 6-OH dopamine both eliminate this blood pressure-elevating effect of chronic episodic hypoxaemia. Using this model, Sprague-Dawley rats have been challenged with both eucapnic hypoxia and asphyxia and failed to show an additional blood pressure elevation above that caused by hypoxia (hypocapnic) alone. It appears that hypocapnic hypoxia creates a maximal stimulus to the sympathetic nervous system to which the addition of hypercarbia does not increase the blood pressure response. An alternative explanation is that the rat has protective mechanisms that limit the diurnal blood pressure response from further increase.
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PMID:An animal model of the relationship between systemic hypertension and repetitive episodic hypoxia as seen in sleep apnoea. 1060 78

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

Sleep has well-recognized effects on breathing, including changes in central respiratory control, airways resistance, and muscular contractility, which do not have an adverse effect in healthy individuals but may cause problems in patients with COPD. Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep. However, sleep studies are usually only indicated in patients with COPD when there is a possibility of sleep apnea or when cor pulmonale and/or polycythemia are not explained by the awake PaO(2) level. Management options for patients with sleep-related respiratory failure include general measures such as optimizing therapy of the underlying condition; physiotherapy and prompt treatment of infective exacerbations; supplemental oxygen; pharmacologic treatments such as bronchodilators, particularly ipratropium bromide, theophylline, and almitrine; and noninvasive positive pressure ventilation.
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PMID:Impact of sleep in COPD. 1067 75

We investigated nocturnal oxygen desaturation (NOD) in 36 patients with stable chronic respiratory disease who were receiving home oxygen, therapy (HOT). Study data included medical history, chest roentgenograms, measurement of daytime arterial blood gases while awake, and spirometry. Each subject underwent full overnight oximetry monitoring. Three patients were excluded from further investigation because of periodic desaturation suggestive of sleep apnea. The remaining 33 subjects were divided into two groups: 21 patients with sequelae of pulmonary tuberculosis (TB-sequela) and 12 patients with chronic obstructive pulmonary disease (COPD). The COPD group was divided into two subgroups according to the Burrows classification (Am Rev Resp Dis. 90: 14-27, 1964): 5 patients with type A (Type A) and 7 patients with type B (Type B) COPD. The percentages of total sleep time with SaO2 < or = 85% (DST 85) and SaO2 < or = 90% (DST 90) were calculated for each subject. NOD was defined as DST 85 > or = 1%. Arterial oxygen partial pressure (PaO2) while awake was > or = 60 Torr in all subjects. No difference was observed in mean awake PaO2 values between the TB-sequela and COPD groups. NOD was detected in 8 TB-sequela patients but in none of the COPD patients. Mean DST 85 and DST 90 values were significantly (p < 0.05) higher for the TB-sequela group than for the COPD group. Of 15 TB-sequela patients who were able to complete spirometry tests, 6 had NOD. All 6 of these patients had hypercapnia while awake (PaCO2 > or = 50 Torr) and reduced vital capacity (< or = 50% predicted). No difference was observed in mean DST 90 or DST 85 values between the TypeA and TypeB COPD subgroups. We conclude that NOD is common in patients with chronic stable respiratory disease treated with HOT despite daytime euoxia. TB-sequela patients with hypercapnia and restrictive ventilatory impairment are at high risk for NOD.
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PMID:[Nocturnal oxygen desaturation during home oxygen therapy in patients with chronic respiratory disease]. 1072 46

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

It is well known that obstructive sleep apnoea is especially frequent in the morbidly obese. In these subjects diurnal chronic hypercapnia, whose mechanism is still debated, may be present. Our study was performed to evaluate the prevalence and the mechanism of diurnal hypercapnia in the morbidly obese affected by obstructive sleep apnoea. From a population referred to our centre because of suspicion of sleep related breathing disorders, we selected 285 subjects without cardiopulmonary, neuromuscular or endocrinological diseases: 89 (36 M and 53 F, aged 46+/-13 years) had body mass index (BMI) > or = 40 kg m(-2) (MO group: morbidly obese subjects) and 196 (99 M and 97 F, aged 48+/-16 years) had BMI <40 kg m(-2) (NMO group: non-morbidly obese subjects). Then the MO group was divided into three subgroups: normocapnic subjects without obstructive sleep apnoea, normocapnic subjects with obstructive sleep apnoea, hypercapnic subjects with obstructive sleep apnoea; while we found no hypercapnic subject without obstructive sleep apnoea. All subjects underwent anthropometric evaluations and bioelectrical impedance analyses, respiratory function tests and arterial blood gas analysis, a modified version of the Sleep and Healthy questionnaire and a full night polysomnography. Our results showed that hypercapnia (PaCO2 > or = 45 mm Hg) associated with obstructive sleep apnoea [respiratory disturbance index (RDI) > or = 10 h(-1)] was found in 27% of the morbidly obese subjects, but only in 11% of the nonmorbidly obese ones (P<0.01). The comparison among the three subgroups, in which we divided the morbidly obese subjects, shows that those with hypercapnia and obstructive sleep apnoea had significantly more important ventilatory restrictive defects [forced vital capacity (FVC)% of pred 73.27+/-14 81 vs. 82.37+/-16.93 vs. 87.25+/-18.14 respectively; total lung capacity (TLC)% of pred 63.83+/-16.35 vs. 79.11+/-14.15 vs. 87.01+/-10.5], a significantly higher respiratory disturbance index (RDI 46.34+/-26.90 vs. 31.79+/-22.47 vs. 4.98+/-3.29) a longer total sleep time with oxyhaemoglobin saturation<90% [total sleeptime (TST)SaO2<90% 63.40+/-33.86 vs. 25.95+/-29.34 vs. 8.22+/-22.12] and a lower rapid eye movement (REM) stage (9.5+/-1.2 vs. 14.0+/-0.9 vs. 17.05+/-1.2) than normocapnic subjects with obstructive sleep apnoea or subjects without obstructive sleep apnoea. The best model to predict PaCO2 resulted from a combination of TSTSaO2<90% (r2 = 0.22, P<0.001), forced expiratory volume in 1 sec (FEV1)% of pred (r2 = 0.09, P<0.01), FVC % of pred (r2 = 0.075, P<0.01). In conclusion our study suggests that diurnal hypercapnia is frequently associated with obstructive sleep apnoea in the morbidly obese without chronic obstructive pulmonary disorder (COPD) and that ventilatory restriction and sleep related respiratory disturbances correlate to diurnal hypercapnia.
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PMID:Prevalence and mechanisms of diurnal hypercapnia in a sample of morbidly obese subjects with obstructive sleep apnoea. 1078 35


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