打鼾与睡眠呼吸暂停低通气综合征的关系研究

目的调查打鼾患者睡眠呼吸暂停低通气综合征的患病率,探讨打鼾与夜间低氧的关系。方法采用流行病调查的方法对克拉玛依市天山社区1121例35岁以上常住居民进行人户睡眠问卷调查及夜间呼吸血氧监测。结果鼾症高危组与鼾症低危组在颈围、腹围、氧减指数、夜间最低氧饱和度、呼吸暂停指数等方面比较差异有统计学意义（P均〈0．05）。鼾症组与非鼾症组在体重指数、颈围、腹围、氧减指数、夜间最低氧饱和度、呼吸暂停指数、低通气指数比较差异有统计学意义（P均〈0．01）。鼾症高危组与低危组间睡眠呼吸暂停低通气综合征的发生率比较差异有统计学意义（P〈0．05）。结论打鼾与睡眠呼吸暂停低通气综合征、夜间低氧相关,睡眠呼吸暂停低通气综合征与鼾症分级有关,颈围和腹围是打鼾和睡眠呼吸暂停低通气综合征的危险因素。     

Oxygen desaturation during sleep as a function of the underlying respiratory disease

Patients with hypoxemia due to respiratory diseases may desaturate further during sleep. A quantitative analysis of this sleep-induced desaturation, simultaneously comparing patients with different respiratory diseases, could identify patient groups especially prone to develop nocturnal hypoxemia. I have therefore compared the changes in oxygenation during sleep in three groups of patients with the same baseline oxygen saturation but with entirely different types of respiratory dysfunction, namely interstitial lung disease (n = 14), chronic obstructive pulmonary disease (n = 29), and scoliosis (n = 10). The patients with scoliosis had considerably larger sleep-induced desaturation than the patients with lung diseases. Their oxygen saturation was also more unstable than that of the others during REM sleep; possibly a consequence of their lower position on the oxyhemoglobin dissociation curve during this sleep stage. The results suggest that sleep studies may be more informative in patients with scoliosis, for example, where a need for nocturnal-assisted ventilation can be revealed, than in patients with lung diseases.     

11O例老年阻塞性睡眠呼吸暂停低通气综合征患者多导睡眠监测及相关分析

目的 加深对老年患者阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apneahypopnea syndrome,OSAHS)特点的认识,提高老年OSAHS诊治水平.方法 对我院睡眠呼吸障碍与鼾症诊治中心诊断的110例老年OSAHS患者的整夜多导睡眠图(PSG)监测资料进行回顾性分析,应用SPSS 18.0统计软件对患者的一般情况、睡眠结构、呼吸暂停和低通气情况、氧减饱和情况以及各指标间可能的相关关系进行统计分析.结果老年OSAHS患者中位快动眼相(rapid eye movement,REM)和非快动眼相(NREM)睡眠时间分别占2.17%和76.73%;中位觉醒指数为45.60次/h.呼吸暂停最长时间为(51.94±22.06)s,中位呼吸暂停平均时间为22.50 s,低通气最长时间为(47.06±12.52)s,低通气平均时间为(21.50±4.63)s.中位呼吸紊乱指数(respiratory disturbance index,RD1)为21.50,RDI 5～20者占46.40%,20～40者占31.80%,＞40者占21.80%.夜间平均血氧饱和度为(93.45±2.81)%,夜间最低血氧饱和度为(76.30±10.50)%,中位氧减饱和指数为31.65次/h.体质指数(BMI)与夜间最低血氧饱和度(r=-0.378,P＜0.01)和夜间平均血氧饱和度(r=-0.355,P＜0.01)呈负相关,与氧减指数呈正相关(r=0.338,P＜0.01);夜间最低血氧饱和度与阻塞性呼吸暂停最长时间(r=-0.47,P＜0.01)、阻塞性呼吸暂停平均时间(r=-0.31 6,P＜0.01)、低通气最长时间(r=-0.293,P＜0.01)和低通气平均时间(r=-0.277,P＜0.01)呈负相关.仰卧位睡眠时中位氧减时间间隔为2.36 min,左侧卧位睡眠时中位氧减时间间隔为11.54 min,右侧卧位睡眠时中位氧减时间间隔为12.45 min,左侧卧位和右侧卧位睡眠时中位氧减时间间隔均长于仰卧位(Z值分别为-6.12和-7.10,均P＜0.01).结论 老年OSAHS患者存在明显的睡眠结构紊乱和睡眠片段化.依据RDI对患者的病情分级,大多数OSAHS患者为轻、中度,但缺氧程度较重,缺氧严重度与BMI和睡眠呼吸事件的持续时间相关,侧卧睡眠时缺氧程度减轻.     

Relationship of ventricular ectopy to nocturnal oxygen desaturation in patients with chronic obstructive pulmonary disease

Sudden death and oxyhemoglobin desaturation are known to occur during sleep in patients with chronic obstructive pulmonary disease. The present study was undertaken to determine the frequency with which nocturnal oxygen desaturation promotes an increase in ventricular ectopic activity, since such a relationship could represent a potential pathophysiologic mechanism for sudden death during sleep. Forty-two clinically stable subjects with moderately severe obstructive airways disease, mean ratio of one-second forced expiratory volume to forced vital capacity = 51 +/- 12 percent, underwent overnight polygraphic sleep study. Oxyhemoglobin saturation was monitored by ear oximetry, and electrocardiographic leads CC5 and CM5 were employed for arrhythmia detection. Premature ventricular complexes were detected in 27 (64 percent) of the subjects and were complex (multifocal, repetitive, or both) in 17. No significant relationship between premature ventricular complex frequency and arterial oxygen saturation was detected for the group as a whole. In part, this result can be attributed to the relatively mild hypoxemic stress experienced by the 22 subjects in whom arterial oxygen saturation remained greater than 80 percent. In contrast, six (30 percent) of the 20 patients who had desaturation to less than 80 percent showed a greater than 150 percent increase in premature ventricular complex frequency with oxygen desaturation. These results suggest that nocturnal hypoxemia, if of sufficient magnitude, is capable of increasing ventricular ectopy during sleep in a substantial number of patients with chronic obstructive pulmonary disease.     

Cerebral oximetry improves detection of sickle cell patients at risk for nocturnal cerebral hypoxia

We previously used cerebral oximetry to identify low cerebral venous oxygen saturation in waking children with sickle cell disease (SCD). Because arterial oxyhemoglobin desaturation is common during sleep in SCD patients, this study compared both waking and sleeping systemic arterial and cerebral venous oxygenation dynamics in children with and without SCD. Seventeen African-American (AA) children with homozygous SCD [8 (4-15) years; 29% male; normal transcranial Doppler velocities] were compared with a control cohort (CON) comprised of six healthy AA children [9 (4-16) years, 33% male]. Standard all-night polysomnographic recordings were performed, including measurement of arterial oxygen saturation by pulse oximetry (SpO(2)). Regional cerebral oxygen saturation (rSO(2)) was measured non-invasively with cerebral oximetry. Intra-cohort comparisons examined the influence of sleep on SpO(2) and rSO(2) in the subjects. Inter-cohort comparisons of SpO(2), rSO(2,) and the rSO(2)/SpO(2) ratio assessed the impact of SCD on systemic and cerebral oxygenation during wakefulness and sleep. Cohort differences in SpO(2) were not statistically significant in either wakefulness or sleep. However, only in the SCD cohort was the magnitude of SpO(2) change statistically significant (P = 0.002). In contrast, both waking and sleep rSO(2) cohort median values did differ significantly [awake: CON 76 (67-86) vs. SCD 62 (58-71), P = 0.01; sleep: CON 65 (60-77) vs. SCD 55 (48-61), P = 0.01)]. The waking rSO(2)/SpO(2) ratio was also significantly lower in the SCD group [CON 0.78 (0.68-0.88) vs. SCD of 0.66 (0.61-0.72); P = 0.015]. During sleep, the ratio was also significantly lower in the SCD group [CON 0.71 (0.66-0.81) vs. SCD 0.59 (0.52-0.65); P = 0.011]. Our findings suggest that SCD patients may be at increased risk of cerebral hypoxia during both wakefulness and sleep.     

Oxygenating mouthguard alleviates hypoxia during gastroscopy.

A randomized study was carried out to determine the effect of oxygen (3 liters/min) via a novel oxygenating mouthguard (Oxyguard) on arterial oxygenation in 242 intravenously sedated patients undergoing gastroscopy. In another group of 21 patients, a randomized crossover study of arterial oxygen saturation using either the standard mouthguard or the oxygenating mouthguard (3 liters/min) was conducted. Significant O2 desaturation (pulse oximeter reading less than 90%) occurred in 25% of patients on room air but only 3% of those on oxygen (p less than 0.001). Severe desaturation (reading less than 85%) occurred in 5% of patients on room air but was prevented by the oxygenating mouthguard. Minimum oxygen saturation levels were significantly higher in patients on oxygen (90.5 +/- 0.3%) than on air (86.5 +/- 0.5%; p less than 0.001). In the crossover group, O2 saturation was uniformly higher in the recordings of all patients using the oxygenating mouthguard. In conclusion, administration of oxygen via the oxygenating mouthguard alleviates hypoxemia during gastroscopy and prevents severe oxygen desaturation. However, hypoxemia may occur even during use of supplemental oxygen. Hence, monitoring of arterial oxygenation is recommended.     

Oxygen saturation with sleep in patients with sickle cell disease

Ear oximetry was used to monitor arterial oxygenation in seven patients who had a history of frequent admissions for sickle cell crisis and were taking narcotic analgesics. Five full-night studies and seven daytime "nap" studies were performed in which sleep state was monitored by electroencephalography, and respiratory rate and tidal volume were monitored by inductance plethysmography. For all patients the mean (+/- SEM) of the median oxygenation values was 93.3% +/- 0.4% during wakefulness and 91.4% +/- 0.8% during sleep. During wakefulness the lowest saturation was 90% +/- 0.5%; during sleep there was a fall in the lowest oxygen saturation to 86.5% +/- 0.9%. In all patients a fall in oxygen saturation was associated with a decrease in respiratory depth without a change in respiratory frequency. The results indicate that in sickle cell disease oxygen saturation is lower during sleep than during wakefulness and that hypoxemia can be attributed to a fall in tidal volume.     

The influence of patent foramen ovale on oxygen desaturation in obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is associated with oxygen desaturation to a varying degree. A patent foramen ovale (PFO) may allow interatrial right-to-left shunting. The hypothesis of the current study was that oxygen desaturation will occur more often, in proportion to the frequency of respiratory disturbances, in OSA subjects with PFO than in those without. In a group of 209 subjects diagnosed with OSA, the proportion of desaturation to respiratory events was calculated as the ratio of oxygen desaturation index (ODI)/apnoea-hypopnoea index (AHI). A total of 15 cases with high proportional desaturation (ODI/AHI >or=0.66) were individually matched with 15 controls with low proportional desaturation (ODI/AHI or=20 bubbles passed over from the right to the left atrium after a single injection. The prevalence of large PFO was nine out of 15 (60%) in the high proportional desaturation group versus two out of 15 (13%) in the low proportional desaturation group. The median number of passing bubbles was positively correlated to minimum oxygen saturation among those with PFO. In conclusion, oxygen desaturation occurs more often, in proportion to the frequency of respiratory disturbances, in obstructive sleep apnoea subjects with a patent foramen ovale than in those without.     

The impact of obesity on oxygen desaturation in patients with sleep apnea/hypopnea syndrome]

We performed a cross-sectional investigation on the impact of obesity on clinical manifestations in patients with obstructive sleep apnea/hypopnea syndrome (SAHS). The subjects were 87 patients who underwent overnight polysomnography with an apnea/hypopnea index (AHI) of 15/h or more. We divided these patients into non-obese (N) and obese (O) groups based on the median value of the body mass index (BMI), 27 kg/m2. Subjective symptoms, sleep quality and AHI were similar in both groups, but every parameter related to oxygen desaturation was worse in group O than in group N. There was no difference in the mean duration of apnea events between the two groups. The rate of fall in oxygen saturation during apnea events was highly correlated to the BMI (r = 0.72; p < 0.00001). Accordingly, we concluded that profound desaturation in group O is due to a rapid fall in oxygen saturation during apnea events compared with group N. Anthropometric measurements revealed that the rate of fall in oxygen saturation was more related to abdominal circumference (AC) than the neck circumference (NC), which is contrasted with the finding that AHI was more related to NC than AC. This fact suggests that abdominal obesity may deteriorate oxygenation during apnea events and may therefore aggravate the risk of cardiovascular disease in patients with SAHS.     

睡眠呼吸紊乱患者的警觉性测定

目的检测几种临床常见的睡眠呼吸紊乱患者的警觉性是否受损。方法前瞻性地对因疑诊而接受全晚睡眠监测的患者,在监测前（傍晚）和监测后（早上）,利用电脑模拟开车试验,以碰撞障碍物的百分率,衡量其警觉性。以等级方差分析检验各组间早晚平均碰撞率（％Ｈｍ）的差异,并将％Ｈｍ与睡眠监测有关参数作等级相关分析。结果正常人和按诊断分组后患者的％Ｈｍ［以中位数（范围）表示］为：正常人（１１名）０．６（０～２．５）;睡眠鼾症（７例）１．１（０．２～２．０）;阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ,２２例）２．２（０．２～７．７）;中枢性睡眠呼吸暂停综合征（ＣＳＡＳ,６例）２．７（０．９～５．４）。除睡眠鼾症组外,各组患者％Ｈｍ均高于正常人（Ｐ＜０．０５）。正常、睡眠鼾症及ＯＳＡＳ三组合并分析表明：％Ｈｍ与睡眠累计低血氧饱和度时间％有相关性（ｒ＝０．４１,Ｐ＜０．０５）而与呼吸停顿／低呼吸指数和觉醒指数无明显相关（ｒ分别为０．２２和０．１０,Ｐ＞０．０５）。结论ＯＳＡＳ和ＣＳＡＳ患者的警觉性下降,睡眠鼾症患者的警觉性大致正常。警觉性受损可能与睡眠时缺氧有关     

阻塞性睡眠呼吸暂停低通气综合征患者夜间缺氧程度的评估

目的 评估阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者的夜间缺氧程度。方法对疑诊有睡眠呼吸障碍的患者215例进行夜间睡眠呼吸监测,计算平均血氧饱和度（AO2）、最低血氧饱和度（LO2）、氧减指数（ODI）、平均氧减饱和度、血氧饱和度低于90％占整个记录时间的百分比（T〈90％）,并进行相关分析。结果 依据所有患者的呼吸暂停低通气指数（AHI）分为AHI正常组（AHI〈5次／h）、轻度OSAHS组（5次／h≤AHI〈15次／h）、中度OSAHS组（15次／h≤AHI〈30次／h）、重度OSAHS组（AHI≥30次／h）,4组A02、L02、ODI、T〈90％差异有统计学意义（P〈0．001）。AHI与A02、ODI、L02、平均氧减饱和度、T〈90％显著相关（r分别为-0．610、0．983、-0．789、0．782、0．821,P=0．001）。结论 OSAHS患者缺氧严重程度的评估需结合ODI、LO2、T〈90％三个指标综合判断．不能仅考虑单一指标．     

Polysomnographic characteristics in patients with Prader-Willi syndrome

To evaluate the occurrence of sleep-disordered breathing and to clarify the characteristics of sleep among patients with Prader-Willi syndrome (PWS). Overnight continuous EEG-polysomnographic studies were performed in 30 patients with PWS (16 males and 14 females; mean age, 7.4 +/- 4.1 years; age range, 1-19 years) unselected for sleep disturbance. The baseline arterial oxygen saturation (SpO2) was 96.6 +/- 0.6%, with a nadir of 77.2 +/- 10.2%. The rapid eye movement (REM) latency was 67.4 +/- 30.0 min. The percent of total sleep time spent in sleep stages 1, 2, slow wave, and REM were 13.1 +/- 8.2%, 41.9 +/- 10.5%, 21.5 +/- 9.4%, and 21.1 +/- 5.7%, respectively. The respiratory disturbance index (RDI) was 5.8 +/- 3.7/hr and desaturation index (DI) was 8.1 +/- 7.3/hr, respectively. Age-adjusted BMI was associated with more severe hypoxemia during sleep (baseline SpO2, r = -0.53, P < 0.01; nadir SaO2, r = -0.65, P < 0.01; RDI, r = 0.37, P < 0.05; DI, r = 0.53, P < 0.01) and more sleep disruption (arousal index, r = 0.46, P < 0.01). There were no significant associations between gender or genotype pattern (deletion vs. uniparental disomy) and the results of polysomnography. Sleep hypoxemia and sleep disruption are more prevalent in patients with PWS than in normal children. Obesity in these patients is associated with more severe sleep-disordered breathing.     

肝硬化失代偿期患者肝储备功能与动脉血氧相关性研究

[目的]探讨肝硬化失代偿期患者动脉血氧分压（PaO2）、氧饱和度（SaO2）和二氧化碳分压（PaCO2）的变化,评价动脉血氧在肝肺综合征（HPS）临床诊断中的价值,为诊断和预防HPS提供理论依据。[方法]应用血气分析仪测定60例肝硬化失代偿期患者（肝硬化组）及同期住院60例非肝硬化失代偿者（对照组）,比较2组的PaO2、SaO2、PaCO2。并比较肝硬化组Child-Pugh为A、B、C间的PaO2、SaO2、PaCO2。[结果]肝硬化组患者低氧血症发生率为48%。①肝硬化组PaO2与对照组PaO2比较P〈0.01,而肝硬化组和对照组SaO2、PaCO2值水平比较差异无统计学意义（P〉0.05）;②肝硬化Child-Pugh A、B、C 3级间PaO2,SaO2值比较差异有统计学意义（P〈0.01）,而3级间PaCO2水平比较差异无统计学意义（P〉0.05）,且PaO2、SaO2值随着Child-Pugh分级的增高呈下降趋势。[结论]肝硬化患者低氧血症发生率高,其发生率随着Child-Pugh分级的增高而呈梯形上升。血气分析对HPS有诊断价值。     

Effect of triazolam on sleep and arterial oxygen saturation in patients with chronic obstructive pulmonary disease

We compared the effects of a placebo with 0.125 and 0.25 mg of triazolam (Halcion) on sleep quality, oximetry, and respiratory events during sleep in ten stable outpatients with chronic obstructive pulmonary disease. The subjects had a forced expiratory volume in 1 s ranging from 17% to 76% of the predicted value (mean +/- SD, 38.1% +/- 19%) and a waking arterial oxygen pressure from 46 to 84 mm Hg (mean +/- SD, 67 +/- 12 mm Hg). Polysomnography was done on three nights within a two-week period after the patients received on a "blinded" basis either placebo or 0.125 or 0.25 mg of triazolam. Triazolam produced improvements in total sleep duration, time spent in stage 2 nonrapid eye movement (NREM) sleep, and subjective of sleep quality. For most patients, there was a nighttime drop in arterial oxygen percentage of saturation (SaO2) in the placebo condition, but triazolam did not cause a significant worsening, of the mean SaO2, minimum SaO2, or the number of apneic and hypopneic events. Across all experimental conditions, we documented little desaturation during wakefulness (mean low, 87.2% +/- 10.2%), more during NREM sleep (mean low, 83.2% +/- 12.6%), and most desaturation in REM sleep (mean low, 80.1% +/- 15.7%). We conclude that single-night use of triazolam improved the quality and duration of sleep in patients with chronic obstructive pulmonary disease. In patients without severe waking hypoxemia and without carbon dioxide retention, triazolam did not increase either nocturnal hypoxemia or respiratory events during sleep.     

Disordered breathing and oxygen desaturation during sleep in patients with chronic obstructive lung disease (COLD).

Seven patients with chronic obstructive lung disease (COLD) were monitored during their overnight sleep to determine the occurrence of disordered breathing and oxygen desaturation. Nasal and oral airflows were sensed by thermistor probes, chest wall movement by impedance pneumography and arterial oxygen saturation by ear oximetry. These variables were correlated with electroencephalographic and electrooculographic tracings. The subjects had a mean base line oxygen saturation of 89.2 per cent and slept an average of 218 minutes. Six of these seven subjects had one to 30 episodes of oxygen desaturation (decrease more than 4 per cent), 4 seconds to 30 minutes in duration, with declines in saturation as great as 36 per cent. In two subjects, saturation dropped to less than 50 per cent. Breathing was disordered in five of the seven subjects and included apnea and hypopnea. Subjects experienced from nine to 37 episodes of disordered breathing. Disordered breathing caused 42 per cent of the episodes of desaturation, all of which were less than 1 minute in duration. The mean maximum decline in saturation was 7.6 per cent. All episodes of desaturation lasting longer than 5 minutes occurred in rapid eye movement (REM) sleep and were not caused by disordered breathing. The mean maximal decrease in saturation was 22 per cent. This study reveals that disordered breathing is common in subjects with COLD and often causes desaturation but that it cannot explain all episodes of sleep desaturation.     

Apnea duration and hypoxemia during REM sleep in patients with obstructive sleep apnea

Nocturnal sleep studies of 12 patients with obstructive sleep apnea and a matched control group of 12 subjects without the sleep apnea syndrome were analyzed to compare arterial oxyhemoglobin saturation (SaO2) during REM and non-REM sleep. Mean percentage of total sleep time spent in REM sleep was not significantly different in patients with obstructive sleep apnea and in subjects without significant apnea (14.2 +/- SEM 2.2 percent in patients vs 12.0 +/- 2.2 percent in nonapnea subjects). Apneas were longer during REM than non-REM sleep in all 12 patients (p less than 0.01). Oxyhemoglobin desaturations were more frequent during REM than non-REM sleep in both apnea patients and the control subjects. In addition, there was a greater mean fall in SaO2 per desaturation episode in both the apnea patients and non-apnea subjects. We conclude: 1) sleep apneas are longer during REM sleep than non-REM sleep in patients with obstructive sleep apnea; 2) hypoxemia is greater during REM sleep than non-REM sleep in subjects with and without the sleep apnea syndrome.     

交感神经活性和血管内皮功能在阻塞性睡眠呼吸暂停低通气综合征合并高血压发病机制中的作用

目的探讨交感神经活性、血管内皮功能在阻塞性睡眠呼吸暂停低通气综合征（OSAHS）合并高血压发病机制中的作用。方法根据整夜多导睡眠监测（PSG）、血压测量和病史采集将93例患者分为：OSAHS血压正常组、OSAHS合并高血压组、高血压不合并OSAHS组和健康对照组。测定PSG当晚睡眠前后血压、血浆去甲肾上腺素、血浆内皮素和血清一氧化氮；收集PSG当晚22点至次晨6点的所有尿液送检尿3-甲氨基4-羟苦杏仁酸（VMA）。结果OSAHS组患者不论有无高血压，各指标变化为：晨起血浆去甲肾上腺素均显著高于睡前，OSAHS合并高血压组升高更明显；醒后去甲肾上腺素与醒后平均动脉压、睡眠呼吸暂停低通气指数（AHI）、氧减次数、氧减指数、睡眠期间血氧饱和度低于90％的时间占总睡眠时间的百分比（T90）呈显著正相关，与睡眠时最低血氧饱和度（minSaO2）和夜间平均血氧饱和度（MSaO2）呈显著负相关；醒后内皮素显著增高、一氧化氮明显下降，而另外两组则相反；醒后内皮素与醒后平均动脉压、AHI、最长呼吸暂停时间、呼吸暂停总时间、氧减次数、氧减指数、T90呈显著正相关，与minSaO2、MSaO2呈显著负相关；醒后一氧化氮与醒后平均动脉压、AHI、最长呼吸暂停时间、呼吸暂停总时间、氧减次数、氧减指数、T90呈显著负相关。与minSaO2、MSaO2呈显著正相关。各组间尿VMA无明显变化。结论在OSAHS患者夜间一过性血压升高和持续性高血压形成方面，交感神经系统活性增强、血管内皮功能紊乱导致的内皮源性舒、缩因子失衡可能起着重要的作用。     

Reactive Oxygen Metabolites (ROMs) as an Index of Oxidative Stress in Obstructive Sleep Apnea Patients

Study Objectives: Obstructive sleep apnea syndrome (OSA) is accompanied by oxygen desaturation and arousal from sleep. Free oxygen radicals are highly reactive molecules which could be produced by the OSA phenomenon of hypoxia/reoxygenation: cyclical alterations of arterial oxygen saturation with oxygen desaturation developing in response to apneas followed by resumption of oxygen saturation during hyperventilation. On the basis of these considerations, it was hypothesized that OSA may be linked to increased oxidative stress. Materials and methods: Twenty-six participants gave an interview during which a physician asked them about their age, smoking habits, and symptoms such as excessive daytime sleepiness and snoring. Physical examination and polysomnography were performed during their hospitalization. Reactive oxygen metabolites (ROMs) were measured in blood samples by the diacron reactive oxygen metabolites (D-ROM) test. Results: Twenty-one out of 26 subjects had an apnea/hypopnea index greater than 5 (OSA group). The measurement of free radicals was high in OSA patients. Furthermore, ROMs values in OSA patients were linearly correlated with the apnea/hypopnea index (R = 0.426; p = 0.042). The predictive value of a positive D-ROM test is 81%. Conclusions: ROMs were elevated in patients with OSA. When OSA was severe, similarly the value of ROMs in blood samples was enhanced, and the probable underlying mechanism for these events is the hypoxia/reoxygenation phenomenon.     

Factors that correlate with sleep oxygenation in children with cystic fibrosis

OBJECTIVE: Cystic fibrosis (CF) patients may develop hypoxemia during sleep. Limited information is available on nocturnal oxygen saturation in CF children with less severe lung disease. The aim of this study was to investigate the degree of nocturnal oxygen desaturation and factors that correlate with nocturnal oxygenation in CF children with normal pulmonary function tests (PFTs) or mild to moderate lung disease. METHOD: Awake resting and post-exercise SpO2 were measured by pulse oximetry. Each patient had overnight oximetry monitorization at home. Six minutes walk test (6MWT), Shwachman-Kulczycki (S-K), Brasfield and computed tomography (CT) scores, blood gas analysis and nutritional status of patients were evaluated. RESULTS: Twenty-four patients with a median age of 9.5 years were included. Nocturnal mean SpO2 did not differ according to the severity of lung disease based on PFT. However, lowest SpO2 obtained was lower in children with both mild and moderate lung disease compared to normals (87.4% vs. 91.7%, respectively, p = 0.009). 95.8% of CF children with normal PFT or mild to moderate lung disease had desaturation events during sleep. Nocturnal mean SpO2 correlated with S-K (Spearman's rho = 0.64, p < 0.0001), Brasfield (Spearman's rho = 0.31, p = 0.007) and CT scores (Spearman's rho = -0.67, p < 0.0001) as well as PaO2 (Spearman's rho = 0.28, p = 0.021), SaO2 (Spearman's rho = 0.28, p = 0.023), z-score of weight (Spearman's rho = 0.23, p = 0.20) and height (Spearman's rho = 0.20, p = 0.30), there was no correlation with 6MWT. CONCLUSIONS: In CF children with normal PFT or mild-to-moderate lung disease, nocturnal oxygenation may correlate with S-K, Brasfield and CT scores as well as PaO2, SaO2, z-score of weight and height.     

Endothelin-1 Levels in Interstitial Lung Disease Patients During Sleep

Background: Hypoxemia stimulates endothelin-1 (ET-1) secretion. The reduction in alveolar ventilation during sleep is considered sufficient to account for the hypoxemia observed in patients with respiratory diseases. Objective: The aim of this study was to evaluate the arterial ET-1 levels and their relationship with pulmonary hypertension in patients with interstitial lung disease (ILD) during sleep. Methods: We examined 38 patients with ILD using formal polysomnography (electroencephalogram, electrocardiogram, airflow, respiratory muscle movement, oximeter) to detect the presence of nocturnal, nonapneic, oxyhemoglobin desaturation. All patients desaturated below a baseline sleep saturation of 90% for 5 minutes or more, reaching a nadir saturation of at least 85%. Each patient had already undergone right heart catheterization with a Swan-Ganz catheter for measuring hemodynamic parameters. Sampling of arterial blood from a radial artery line for determination of blood gases and ET-1 values was performed simultaneously, after 5 minutes of the first desaturation. Results: At rest, arterial ET-1 levels were higher in ILD patients (1.73 ± 0.37 mgr/mL) than in controls (1.22 ± 0.15 mgr/mL) (p < 0.001). Also, the patients with pulmonary hypertension (Pa > 20 mm Hg) presented significantly higher arterial ET-1 levels (1.86 ± 0.32 mgr/mL) than those without pulmonary hypertension (1.31 ± 0.13 mgr/mL) (p < 0.001). Arterial ET-1 levels were significantly correlated with mean pulmonary arterial pressure (PAP) (r = 0.749, p < 0.001), and arterial oxygen partial pressure (PaO₂) (r = 0.79, p < 0.001). At sleep, during desaturation, arterial ET-1 levels significantly increased in all patients (2.46 ± 0.13 mgr/mL) as compared with resting values (p < 0.001). Arterial ET-1 levels were significantly correlated with PAP (r = 0.657, p < 0.001) and PaO2 (r = 0.93, p < 0.001). Conclusions: According to our study, arterial ET-1 is markedly increased in ILD patients, especially in those with pulmonary hypertension.