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)

Oxyhemogloblin affinity (P50 at pH 7.4, PaCO2 = 40 mm Hg, temperature = 37 degrees C) and 2,3-DPG concentration were assessed in 15 nonsmokers (14 men and one woman 46 to 63 yr of age) with sleep apnea syndrome (SAS) and in 10 normal subjects (eight men and two women 22 to 48 yr of age). In patients with SAS, mean nocturnal apnea index was 46 +/- 20/h, and mean nocturnal SO2 was 86 +/- 6% versus 94.6 +/- 1.8% during the daytime. Daytime mean P50 of the patients was 28.5 +/- 1.2 mm Hg versus 27.1 +/- 0.3 mm Hg in the normal subjects (p less than 0.05). Daytime mean 2.3-DPG was 1.23 +/- 0.25 moles DPG/mole hemoglobin versus 0.80 +/- 0.15 (p less than 0.05). Significant correlations were found in patients between P50 and mean nocturnal SO2 (r = -0.62, p less than 0.01) and between P50 and 2,3-DPG (r = 0.68, p less than 0.01). The measurements were repeated in five patients after surgical or positive-pressure treatment. P50 and 2,3-DPG both decreased and returned to normal values. In conclusion, the oxyhemoglobin dissociation curve is shifted to the right in patients with SAS and there is an increase in 2,3-DPG. These could be protective mechanisms against the development of polycythemia, pulmonary hypertension, and cor pulmonale.
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PMID:Decreased oxyhemoglobin affinity in patients with sleep apnea syndrome. 190 Apr 1

Morbid obesity is often associated with severe respiratory insufficiency, commonly known as the pickwickian syndrome. This can be divided into the following two primary breathing disorders which can affect patients alone or in combination: the obstructive sleep apnea syndrome (SAS); and the obesity-hypoventilation syndrome (OHS). Thirty-eight (14 percent) of 263 morbidly obese patients with respiratory insufficiency of obesity underwent gastric surgery for weight reduction. Ten had OHS, nine has SAS, and 19 had both. Of these patients, one died of postoperative complications, one died at five weeks with an inconclusive autopsy, one was lost to follow-up, and the time since surgery was too short (less than three months) in three. A total of 30 patients lost 45 +/- 25 percent (p less than 0.0001) of excess body weight within 3 to 12 months following surgery, when repeat pulmonary studies were done. Most patients continued to lose additional weight until two years, when they had lost 62 +/- 26 percent of excess weight. Nine patients failed initial surgery (gastroplasty); seven of these were successfully converted to gastric bypass. Weight loss was associated with a significant decrease in the percentage of sleep apnea from 44 +/- 15 to 8 +/- 11 (p less than 0.0001). In patients with OHS, the arterial oxygen pressure (PaO2) increased from 53 +/- 9 to 68 +/- 11 mm Hg (p less than 0.0001), and the arterial carbon dioxide tension decreased from 51 +/- 7 to 41 +/- 4 mm Hg (p less than 0.0001). Pulmonary function tests in the patients with OHS revealed significant increases, as a percentage of predicted normal, in the forced vital capacity, forced expiratory volume in one second, expiratory reserve volume, functional residual capacity, and total lung capacity. Secondary polycythemia, defined as a hemoglobin level greater than 16 g/dl associated with a PaO2 less than 60 mm Hg, was noted in 13 of 29 patients with OHS. This fell from 16.9 +/- 1.1 to 14.9 +/- 1.7 g/dl (p less than 0.001) after weight loss and improved pulmonary function.
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PMID:Gastric surgery for respiratory insufficiency of obesity. 372 Mar 90

We examined the clinical and respiratory physiologic characteristics of 18 patients in whom a diagnosis of central sleep apnea syndrome was established by overnight polysomnographic studies. The patients could be readily divided into 2 groups on the basis of physiologic and clinical criteria. Five patients had an awake arterial PCO2 (PaCO2) of 53 +/- 4 (SEM) mmHg in the absence of intrinsic bronchopulmonary disease, a ventilatory response to CO2 of 0.6 +/- 0.2 L/min/mmHg, and a hemoglobin concentration of 180 +/- 6 g/L. Their clinical course was dominated by recurrent episodes of respiratory failure. In contrast, the other 13 patients had an awake PaCO2 of 35 +/- 1 mmHg (p less than 0.001), a CO2 response of 2.9 +/- 0.4 L/min/mmHg (p less than 0.005), and a hemoglobin concentration of 150 +/- 5 g/L (p less than 0.005). Clinically, they presented with features typical of sleep apnea; none had a history of respiratory failure. Despite the clinical and physiologic differences between the 2 groups, there were no differences between them in the frequency or duration of nocturnal apneic events or in sleep architecture. The findings indicate that the central sleep apnea syndrome is not a homogeneous disease entity. Rather, it includes 2 groups of patients that are clinically and physiologically distinct, with 1 group chronically hypoventilating and the other group either chronically hyperventilating or ventilating normally.
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PMID:Clinical and physiologic heterogeneity of the central sleep apnea syndrome. 374 Jun 46

The percentage of subjects with sleep apneic activity was significantly greater in a group of 60 healthy subjects who were 50 yr and older compared with a control group of 69 subjects who were younger than 50 yr. Sixteen of the older subjects (26.7%) and six of the younger subjects (8.7%) met the criteria for sleep apneic activity, i.e., 3-29 episodes per night. However, only one of the older subjects (1.7%) had enough sleep apneic activity (30 or more episodes in a night) to meet the definition of the condition of sleep apnea. In both age groups, sleep apneic activity (SAA) was slightly more prevalent in males than females. Older subjects with SAA were not significantly heavier than those without SAA but were so when compared with the younger subjects with SAA. In the 29 older subjects for whom hemoglobin O2 saturation (Sao2) was recorded, those with SAA had a significantly lower mean minimum Sao2 value (87%) than those without (92%).
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PMID:Sleep apneic activity in older healthy subjects. 399 24

Sleep apnea syndromes and nonapneic arterial oxygen desaturation during sleep are reported more commonly in men than in women. Because men have recently been shown to have a considerably reduced hypoxic ventilatory response (HVR) during sleep, we questioned if this finding would apply to women as well. Accordingly, we measured isocapnic hypoxic responsiveness in 6 normal women during wakefulness and all stages of sleep during both follicular and luteal phases of the menstrual cycle. During non-REM sleep, women were found to maintain their waking levels of HVR, measured as the slope of the relationship between ventilation and decreasing hemoglobin saturation. Hypoxic ventilatory response fell to 70% of the awake value during REM sleep, which was a significant change (p less than 0.05). Although HVR tended to be greater in the luteal than in the follicular phase of the menstrual cycle, both awake and asleep, this was significant only in Stage 2 sleep (p less than 0.05). When compared with recently reported men studied in this laboratory, these women demonstrated significantly less awake HVR even when corrected for body surface area (p less than 0.05). During sleep men and women had similar hypoxic responses, although this represents a considerable decrement in the awake response in the men and little change in the women. How these findings relate to the observed sexual differences in "sleep disordered breathing" is speculative.
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PMID:Hypoxic ventilatory response during sleep in normal premenopausal women. 712 40

Sleep apnea syndrome (SAS) consists of nocturnal snoring interrupted by obstructive apnea and of diurnal symptoms like hypersomnolence as a consequence of sleep fragmentation. Cardiovascular morbidity and mortality associated with this syndrome justify early detection and appropriate treatment. Polysomnography is still a frequently used method for early detection; however, several disadvantages like duration, discomfort and expense led to a search for alternatives. Since the beginning of the eighties, oximetry allows recording of nocturnal oxygen saturation of hemoglobin even at home. Nocturnal oximetry reveals O2-desaturation associated with apnea and thus permits often to diagnose or exclude SAS. Diagnosis of SAS is made when at least 20 desaturations per hour with an amplitude of at least 4% are recorded. On the other hand, normal nocturnal oximetry nearly excludes SAS. In those cases where nocturnal oximetry is not diagnostic, polysomnography remains the method of choice. Departing from published work, a model for SAS detection, based mainly on nocturnal oximetry, is proposed.
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PMID:[Screening for sleep apnea syndrome]. 793 64

This study addresses the hypothesis that patients with obstructive sleep apnea, who exhibit recurrent episodes of oxygen desaturation at night, have higher hematocrit levels than nonapneic control subjects. We prospectively studied 624 patients referred to the sleep disorders center at St. Michael's Hospital because of suspicion of sleep apnea. All patients had nocturnal polysomnography and measurements of hematocrit level, hemoglobin value, WBC count, and platelet count. Smoking history and awake oxygen saturation (SaO2) was recorded in all of them. Nocturnal oxygenation was assessed using three indices: lowest nocturnal SaO2 (LoSaO2), mean nocturnal SaO2 (MnSaO2) and percent of total sleep time spent at SaO2 lower than 85 percent (TST85%). Patients with TST85% in the lowest quartile (TST85% = 0) had minimally lower hematocrit levels than patients with TST85% in the highest quartile (8 < or = TST85% < or = 90): 0.41 +/- 0.03 vs 0.40 +/- 0.02 in female subjects and 0.45 +/- 0.05 vs 0.43 +/- 0.05 in male subjects, respectively (p < 0.05). Multiple linear regression analysis revealed that MnSaO2, age, and pack-years of smoking were significant predictors of hematocrit level, but they accounted for only 9 percent of the variability in hematocrit level (multiple R2 = 0.087; p < 0.05). We conclude that intermittent nocturnal hypoxemia during episodes of apnea does not lead to clinical polycythemia, but is associated with minor elevations in hematocrit value. These small elevations are unlikely to be useful as markers of hypoxic stress associated with sleep apnea.
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PMID:Hematocrit levels in sleep apnea. 808 60

We examined the relationship between daytime symptoms and respiratory disturbance indices during sleep in 60 patients with sleep apnea syndrome who had an apnea index of more than 5/hr for at least one night. Daytime hypersomnolence, morning headache, and a history of traffic accidents did not correlated strongly with apnea index or with nocturnal desaturation. The same was true of daytime blood pressure and nocturnal micturition. Both hemoglobin concentration and the mean pulmonary arterial pressure in the daytime correlated significantly with indices of nocturnal desaturation and not with apnea index, but this might reflect the positive correlation between those variables and the base-line level of daytime PaO2, in which case it would not be a direct consequence of nocturnal desaturation. These data suggest that diagnostic criteria should not be based on apnea index or desaturation alone. Long-term follow-up data on Japanese patients is needed to establish more rational diagnostic criteria and stage classification for sleep apnea syndrome.
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PMID:[Current problems in the Diagnosis and stage classification of sleep apnea syndrome]. 875 84

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.
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PMID:Effects of alcohol on sympathetic activity, hemodynamics, and chemoreflex sensitivity. 918 Jun 29

Twenty patients of interstitial lung disease (ILD) and same number of healthy adults were selected to monitor arterial hemoglobin oxygen saturation (SaO2) breathing pattern and arrhythmias during sleep. The maximum fall in SaO2 during sleep was 13.1% (10-16%) in ILD patients as compared to 4.8% (3-6%) in controls and the difference was significant (p < 0.005). The ILD patients spent 16.9% of mean total sleep time (TST) below 85% SaO2 and 0.7% of mean TST below 80% SaO2 whereas none of the healthy subjects had SaO2 below 90% during sleep. These patients had more disturbed sleep than controls. Abnormally high breathing frequency demonstrated by ILD patients while awake, was not altered during sleep. Both tidal volume (VT) and minute ventilation (Vmin) decreased by 6.6% and 11.5%, respectively in ILD patients during sleep though it was not significant (p > 0.25) statistically. The respiratory drive was declined during sleep in ILD patients. The percent of tidal volume contributed by rib cage (% RC) lessened during sleep in all the subjects. The ratio of the total excursion of the rib cage and abdomen during inspiration without considering the direction of movement, divided by tidal volume (TCD/VT) revealed asynchronous breathing in ILD patients during sleep. Arrhythmias were found in 6 (30%) of ILD patients and 4 (20%) of control subjects. Observed apnea-hypopnea did not qualify for sleep apnea syndrome in any case.
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PMID:Study of oxygen saturation, breathing pattern and arrhythmias in patients of interstitial lung disease during sleep. 935 49


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