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)

We studied the influence of hypoxia due to sleep apnea on testosterone (T) secretion. It was conducted on the basis of an idea that sustained hypoxia may depress T secretion. The subjects consisted of 15 male patients with no drug administration whose complaints were snoring and/or obesity. The subjects participated in a sleep study on two consecutive nights. During the first night we collected blood samples starting every 4 hours from 10 PM via a catheter and measured T. From the data of the second night, we calculated total desaturation time with more than 4% from the baseline SaO2. According to the amount of this desaturation time, the subjects were divided into 2 groups; desaturation time less than 80 min in group 1 and longer in group 2, respectively. The peak value was seen at 6 AM in group 1 and at 10 AM in group 2. We investigated the correlation between the ratio of T10/T6, which is the ratio of T level at 10 AM to that at 6 AM, and parameters of sleep disorders related to oxygen desaturation. Total 4% desaturation time in total sleep period and non REM period significantly correlated with this ratio. From the diagram illustrating the correlation between the ratio and total 4% desaturation time in total sleep period, we could assume that if the ratio is beyond 1, the subject may have had more than about 80 min of total 4% desaturation time.
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PMID:[Prediction of the degree of nocturnal oxygen desaturation in sleep apnea syndrome by estimating the testosterone level]. 261 9

Thirty-four patients (32 male, 2 female; mean age 53 +/- 7 years) with confirmed sleep apnea syndrome (SAS) were studied before and after uvulopalatopharyngoplasty (UPPP). Clinical symptoms were tiredness, excessive daytime sleepiness and snoring. All patients were overweight. Patients underwent a thorough physical and oropharyngeal examination and polysomnography before and 3 months after surgery. On the basis of post-operative results, patients are divided into 3 groups: --group 1: 16 cured patients: apnea index (A.I./h) 38 +/- 17 before and 4.4 +/- 4 apneas/h sleep after surgery. Improved nocturnal hypoxemia: mean minimum oxyhemoglobin saturation (SAO2) before and after UPPP in NREM sleep 83 +/- 4% v. 90 +/- 4% in REM sleep 76 +/- 11% v. 85 +/- 7%. Uninterrupted sleep is restored; --group 2: 8 improved patients: A.I./h of 64 +/- 11 before and 20 +/- 6 after UPPP: improved nocturnal hypoxemia: mean minimum SAO2 in NREM sleep 74 +/- 10% before and 86 +/- 6% after UPPP: in REM sleep 59 +/- 9% before and 79 +/- 6% after UPPP, lower amount and percentage of fragmented sleep; --group 3: 10 non-improved patients: A.I./h unchanged 55 +/- 22% before and 50 +/- 20% after UPPP. Persistent nocturnal hypoxemia: mean minimum SAO2 in NREM sleep 76 +/- 13 before and 81 +/- 12% after UPPP: in REM sleep 63 +/- 16% before and 65 +/- 24% after UPPP. Sleep remains fragmented. In this last group patients are more overweight and all suffer from severe SAS with greater nocturnal oxyhemoglobin desaturation. Surgical treatment by UPPP is shown to be effective for 70% of our patients. Better results are obtained when SAS is less severe and overweight less important.
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PMID:[Efficacy of uvulopalatopharyngoplasty (UPPP) and modifications in sleep structure in the sleep apnea syndrome (SAS)]. 261 54

In 8 patients with severe sleep apnea syndrome we have studied the immediate effect of nasal continuous positive airway pressure. A good adaptation to the machine during their stay at the laboratory and the beneficial immediate effect on somnolence was observed. There was found a better efficiency of sleep, shortening of latency, decrease of stage 1, increase of REM and shortening of the latency of REM (rebound of REM sleep). Significant correlations were found between the needed pressure to eliminate apneas and the proportion of stage 1 (r = 0.83), of REM stage (r = 0.72) and stage 2 (r = -0.84) of basal night sleep.
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PMID:[Immediate effect of nasal continuous positive pressure in the treatment of obstructive sleep apnea]. 266 56

Seventeen patients who were suspected of having hydrocephalus, because of ventricular dilation from various causes, were included in this study of the pathophysiologic basis of the appearance of pressure waves (PWs). Pressure waves accompanied by apnoeas originated in arousal responses in the resting state of these patients. Frequent fits of apnoea were included in the entire sleep apnoea syndrome. Most pressure waves characteristically appeared in the state of non-REM sleep. During the appearance of such pressure oscillations, intracranial pressure was elevated transiently. This coincidence in the appearance of pressure oscillations with sleep apnoea was the most characteristic pathophysiologic result from this polygraphic study of the patients.
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PMID:Pressure wave with apnoea evaluated by sleep level in patient with ventricular dilation. 290 23

Sleep onset during the multiple sleep latency test was scored by three criteria for 21 patients with narcolepsy and 21 patients with obstructive sleep apnea: a single epoch of stage 1, three consecutive epochs of stage 1, and a single epoch of stage 2 or REM. Mean sleep latency for both groups was predictably shortest using a single epoch of stage 1 and longest using a single epoch of stage 2 or REM. All estimates of sleep latency were highly correlated. It was concluded that a single epoch of any stage of sleep is an appropriate measure of sleep latency for patients with narcolepsy, although a modified scoring system should be developed for patients with sleep apnea. The obstructive apneic episodes prevented or delayed sleep onset on 4.8% to 33.3% of trials depending on the specific criteria used to determine sleep latency. Such apnea-related interruptions to sleep should be taken into account when assessing daytime somnolence in patients with sleep apnea.
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PMID:Determination of sleep latency in polysomnographic evaluations of daytime somnolence in patients with sleep apnea and patients with narcolepsy. 292 26

The influence of a constant increase in functional residual capacity on apnoea characteristics was studied in patients with the sleep apnoea syndrome. Pulmonary inflation was achieved by applying a continuous negative extrathoracic pressure into a Poncho type respirator. Nine patients slept in the Poncho for two consecutive nights, negative extrathoracic pressure being applied during the second night. There was no difference in the total sleep time, its composition within the different sleep stages, the apnoea and apnoea-hypopnoea indices, or the sleep time spent in apnoea between the two nights. The mean (SD) apnoea duration increased with negative extrathoracic pressure from 25.3 (2) to 30.5 (3) seconds (p = 0.003) and time spent in obstructive apnoea (percentage of apnoea time) from 56 (13) to 75 (8) (p = 0.02). The mixed apnoea time (%) decreased from 37 (7) to 21 (7) (p = 0.02). Despite the increase in apnoea duration, less time was spent below each oxygen saturation value during negative extrathoracic pressure. The results were similar for apnoeic episodes during non-REM (non-rapid eye movement) sleep, whereas no significant modifications were seen during REM sleep. It is concluded that the composition of apnoea time and resulting oxygen desaturation are influenced by lung volume.
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PMID:Influence of lung volume in sleep apnoea. 292 88

To test the hypothesis that endogenous opiates play a role in the etiology of the sleep apnea syndrome, we administered naloxone, an opiate antagonist, to ten obese humans with sleep apnea. On two separate nights we measured the frequency and severity of sleep apnea during naloxone infusion vs saline control infusion. The number of oxyhemoglobin desaturation episodes was not significantly lowered but the average maximal oxyhemoglobin desaturation fell significantly (P less than 0.01) with naloxone. The desaturation index (average maximal oxyhemoglobin desaturation times desaturations per hour) fell by 21 percent (P less than 0.05) on the night of naloxone infusion. Nine of the ten patients had a lower desaturation index with naloxone. REM sleep decreased by 80 percent (P less than 0.05) in the subjects in whom it was measured. We conclude that opiate antagonists hold promise in the treatment of sleep apnea and that the endogenous opiate system may be involved in the production of sleep apnea.
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PMID:Naloxone improves sleep apnea in obese humans. 293 47

We report on 2 children aged 13 and 14 months with congenital central alveolar sleep apnea which showed depression of respiratory drive during sleep resulting from dysfunction of central chemoreceptors. Hypoventilation was found to be more severe during NREM sleep (minimum of alveolar ventilation in stages 3/4) than during REM sleep. During NREM sleep arousal responses to hypoxia proved to be an important factor in influencing the level of alveolar ventilation and in preventing fatal asphyxia.
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PMID:[Regulation of respiration during sleep in congenital central sleep apnea]. 309 60

A 41-year-old man developed sleep apnea following abrupt cessation of amitriptyline. Cessation of antidepressants may result in excessive release of acetylcholine, which increases REM sleep. This in turn increases disordered breathing time and decreases nocturnal oxygenation. Sleep apnea did not recur when amitriptyline was reinstated and later gradually discontinued.
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PMID:Sleep apnea following withdrawal of amitriptyline. 324 16

This review summarizes briefly the present knowledge on sleep-related factors in ischaemic heart disease. A marked circadian rhythm in the frequency of onset of acute myocardial infarction has been found, but the exact mechanism is not known. The circadian variation is possibly explained by several mechanisms. The best documented is sleep apnoea syndrome, which seems to be a risk factor for ischaemic heart disease and stroke. Stressful REM-sleep seems to be potentially arrhythmogenic in patients with decreased cardiopulmonary function. The role of coronary spasm, increased thrombocyte aggregation and mental stress in sleep disorders is still poorly understood.
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PMID:Cardiovascular stress and sleep. 331 Aug 37


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