经鼻持续正压通气治疗阻塞性睡眠呼吸暂停低通气呼吸综合征对于血清S100A12表达的影响

目的：研究在阻塞性睡眠呼吸暂停低通气呼吸病的相关治疗方法里,使用经鼻持续正压通气的治疗方式对于血清钙粒蛋白(S100A12)表达的影响。方法：将172个患有阻塞性睡眠呼吸障碍的病人随机分组,其中治疗组与对照组各86例,治疗组给予经鼻持续正压通气治疗,对照组给予药物雾化吸入治疗,治疗周期都为4周。结果：治疗组与对照组治疗后血清S100A12表达值分别为24.98±7.44 ng/ml和32.98±4.98 ng/ml,都明显低于治疗前的45.39±7.12 ng/ml和45.99±6.33 ng/ml(P<0.05),同时组间对比差异明显(P<0.05)。两组治疗后的FEV1和FEV1/FVC值都明显高于治疗前,对比差异明显,同时治疗后治疗组的FEV1和FEV1/FVC值明显高于对照组(P<0.05)。经过相关治疗之后,两组患者体内动脉血氧指数提高,在呼吸暂停低通气指数方面有所降低,和患者治疗之前的数值相比较,P<0.05即指差异明显,同样差异明显的还有两组间的数值对比。两组治疗后的睡眠有效率与睡眠潜伏期都明显提高(P<0.05),同时治疗后治疗组的睡眠有效率与睡眠潜伏期明显高于对照组(P<0.05)。结论：经鼻持续正压通气治疗阻塞性睡眠呼吸暂停低通气呼吸综合征能有效改善睡眠与低氧血症状况,有利于降低血清S100A12表达,从而促进肺功能的恢复。     

Erythropoietin and obstructive sleep apnea

OBJECTIVE: We tested the hypothesis that repetitive severe hypoxemia resulting from obstructive sleep apnea would increase serum erythropoietin, and that this increase would be attenuated by effective treatment of obstructive sleep apnea. METHODS: We studied healthy untreated patients with obstructive sleep apnea (18 severe and 10 very mild) before and after acute treatment with continuous positive airway pressure, and 12 healthy control subjects free of obstructive sleep apnea. RESULTS: Baseline erythropoietin levels before sleep were similar in the obstructive sleep apnea and control groups. However, erythropoietin levels increased (by 20%, P =.037) in patients with severe obstructive sleep apnea after 3.5 hours untreated (lowest O2, 77% +/- 3%), and decreased after 4 hours of continuous positive airway pressure treatment (P =.001). Erythropoietin responses in patients with severe obstructive sleep apnea were different (F = 4.0, P =.03) from controls, in whom erythropoietin levels remained stable throughout the night (P =.94). Erythropoietin responses were similar in very mild obstructive sleep apnea and controls (P =.58). CONCLUSIONS: Our results indicate that untreated severe obstructive sleep apnea results in increased erythropoietin, which decreases after continuous positive airway pressure treatment. Increased erythropoietin may be a potential reversible mechanism to explain the association between obstructive sleep apnea and cardiovascular disease.     

Neuroendocrine changes in sleep apnea

PURPOSE OF REVIEW: To review recent investigations examining the effects of neuroendocrine changes in obstructive sleep apnea. RECENT FINDINGS: Gonadal hormones have long been implicated in the pathogenesis of obstructive sleep apnea. Recently, exogenous testosterone has been shown to exacerbate obstructive sleep apnea, whereas hormone replacement therapy in menopausal women may be protective in obstructive sleep apnea. Effective treatment of obstructive sleep apnea with nasal continuous positive airway pressure has been associated with improved insulin sensitivity and testicular function in individuals with obstructive sleep apnea. SUMMARY: It is important to consider the potential development of sleep apnea in any patient who has an endocrine disorder or is receiving certain hormonal therapies. Effective assessment and management of obstructive sleep apnea with nasal continuous positive airway pressure may lead to a reduction in insulin resistance and hypertension as well as other markers of vascular risk in patients with metabolic syndrome.     

Sustained effect of continuous positive airway pressure on baroreflex sensitivity in congestive heart failure patients with obstructive sleep apnea

BACKGROUND: Patients with either heart failure or obstructive sleep apnea have a reduced baroreflex sensitivity for heart rate, a sign of poor prognosis. We previously demonstrated that nocturnal application of continuous positive airway pressure to heart failure patients with obstructive sleep apnea increased baroreflex sensitivity acutely, but it is not known whether these effects persist into wakefulness. OBJECTIVE: To determine whether treating obstructive sleep apnea in heart failure patients with continuous positive airway pressure improves baroreflex sensitivity during wakefulness. METHODS: Spontaneous baroreflex sensitivity was assessed during wakefulness in 33 heart failure patients (left ventricular ejection fraction < or = 45%) with obstructive sleep apnea (apnea-hypopnea index > or = 20). Subsequently, baroreflex sensitivity was reassessed 1 month after patients were randomly allocated to nocturnal continuous positive airway pressure treatment or no treatment (control). RESULTS: Compared with the 14 control patients, the 19 continuous positive airway pressure-treated patients experienced a greater increase in baroreflex sensitivity [median, (25%, 75%)] [from 5.4 (2.2, 8.3) to 7.9 (4.4, 9.4) ms/mmHg; P = 0.01] and left ventricular ejection fraction (P < 0.001). In addition, daytime systolic blood pressure and heart rate decreased more in the continuous positive airway pressure group (from 122 +/- 15 to 113 +/- 12 mmHg; P = 0.02, and from 66 +/- 8 to 62 +/- 8 bpm; P < 0.001, respectively) than in the control group. CONCLUSION: Treatment of coexisting obstructive sleep apnea by continuous positive airway pressure in heart failure patients improves baroreflex sensitivity during wakefulness in addition to improving left ventricular ejection fraction and lowering blood pressure and heart rate. These data indicate that the improved autonomic regulation of heart rate in heart failure patients treated for obstructive sleep apnea during sleep persists into wakefulness.     

Sympathetic activity is reduced by nCPAP in hypertensive obstructive sleep apnoea patients.

There is increasing evidence that nasal continuous positive airway pressure (nCPAP) lowers blood pressure in obstructive sleep apnoea (OSA) patients, not only during sleep but also in the daytime. However, both the mechanisms of blood pressure reduction and the considerable differences in the magnitude of the effect in the studies presented to date are not fully understood. Therefore, the authors prospectively studied the effect of nCPAP on noradrenaline plasma levels (NApl), blood pressure and heart rate (HR) in 10 normotensive and eight hypertensive OSA patients before and after 41.6 +/- 16.9 days of nCPAP therapy. Polysomnography and invasive blood pressure were continuously monitored over 24 h in the supine position before and with nCPAP. NApl were analysed every 15 min. In hypertensives, nCPAP reduced NApl by 36 +/- 25%, lowered mean arterial blood pressure substantially (night-time: -8.89 +/- 14.09 mmHg; daytime: -7.94 +/- 10.47 mmHg) and decreased HR by 6.6 +/- 5.4 beats x min(-1), whereas in normotensives there were only minor changes. The decrease in heart rate was associated with a decrease in mean arterial blood pressure and noradrenaline plasma levels, suggesting a causal effect of nasal continuous positive airway pressure therapy. This nasal continuous positive airway pressure effect occurs mainly in hypertensive obstructive sleep apnoea patients, whereas the effect is small in normotensives. This may explain, at least in part, some of the discrepant results in previous treatment studies.     

Effects of continuous positive airway pressure versus supplemental oxygen on 24-hour ambulatory blood pressure

Obstructive sleep apnea (OSA) is associated with recurrent episodes of nocturnal hypoxia and increased risk for development of systemic hypertension. Prior studies have been limited, however, in their ability to show reduction in blood pressure after continuous positive airway pressure (CPAP) therapy, and the effect of supplemental oxygen alone on blood pressure in OSA has not been evaluated. We performed a randomized, double-blind, placebo-controlled study comparing the effects of 2 weeks of CPAP versus sham-CPAP versus supplemental nocturnal oxygen on 24-hour ambulatory blood pressure in 46 patients with moderate-severe OSA. We found that 2 weeks of CPAP therapy resulted in a significant reduction in daytime mean arterial and diastolic blood pressure and nighttime systolic, mean, and diastolic blood pressure (all Ps <0.05). Although nocturnal supplemental oxygen therapy improved oxyhemoglobin saturation, it did not affect blood pressure. We conclude that CPAP therapy reduces both daytime and nighttime blood pressure in patients with OSA, perhaps through mechanisms other than improvement of nocturnal oxyhemoglobin saturation.     

Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP.

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.     

Overnight nasal CPAP improves hypersomnolence in sleep apnea

Eleven adult men with sleep apnea underwent nocturnal polysomnography on two successive nights. The first study, done without NCPAP, served as the control. The second (treatment) was done with the application of 7.5 to 15 cm H2O nasal continuous positive airway pressure (NCPAP). A subjective sleepiness index (SSI) was noted upon awakening from each night of polygraphic recording. During the control night, the mean frequency of apnea episodes/sleep hr was 35.95 +/- 4.5 SE, and the mean duration was 28.68 +/- 2.7 sec. Mean frequency of disorder of breathing (DOB) episodes/sleep hr was 19.25 +/- 6.2 and mean duration of DOB episodes was 23.1 +/- 2.8 sec. During the treatment night, all obstructive apnea episodes were abolished. During the control night, the mean decrease in arterial oxygen saturation during obstructive apnea episodes was 11.2 +/- 1.9 percent and the mean lowest saturation was 67.6 +/- 4.0 percent. NCPAP eliminated arterial oxygen desaturation. While 44.5 +/- 5.7 percent of total sleep time was spent in either apnea or disordered breathing during the control night, NCPAP decreased this to 0.73 +/- 0.3 percent. In addition to the improvement in respiration during sleep, SSI decreased from a mean of 3.73 +/- 0.49 after the control night to 1.64 +/- 0.24 after treatment, reflecting an improvement in daytime hypersomnolence. We conclude that nasal CPAP is effective in eliminating obstructive apnea episodes, and results in a marked decrease in daytime hypersomnolence after one treatment night.     

Assessment of continuous positive airway pressure treatment in obstructive sleep apnea syndrome using 24-hour urinary catecholamines

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is related to diurnal sympathetic hyperactivity and increased blood pressure, both factors that are likely to lead to the development of cardiovascular disease. HYPOTHESIS: The study investigated whether 24-h urinary catecholamines would reflect the effect of obstructive sleep apnea on autonomic activity. METHODS: Standard polysomnography was performed in 17 patients with OSAS (age 53.7 +/- 13.5 years, mean +/- standard deviation). The number of apnea/hypopnea episodes per hour of sleep (apnea/hypopnea index [AHI]); number of oxygen desaturation episodes per hour (desaturation index [DSI]); arousals per hour (arousal index); lowest oxygen saturation (lowest SpO2); and percentages of stages 1, 2, 3/4, and rapid eye movement sleep (% stage 1, -2, and -3/4, and % REM, respectively) were measured. Overnight continuous positive airway pressure (CPAP) titration was performed the night after the baseline sleep measurements had been taken. Twenty-four-hour urinary adrenaline and noradrenaline were also examined. RESULTS: During the CPAP treatment, both 24-h urinary adrenaline and noradrenaline were significantly lower compared with natural sleep. Continuous positive airway pressure significantly decreased the AHI, DSI, % stage 1, and arousal index and significantly increased the lowest SpO2. There were no significant differences in % stage 2, % stage 3/4, and % REM between before and during CPAP treatment. Multiple analysis of covariance tests revealed that lowest SpO2 was the most important factor for increasing 24-h urinary noradrenaline levels (F = 4.75, p = 0.048). CONCLUSIONS: One night CPAP treatment could improve autonomic dysfunction. The assessment of 24-h urinary noradrenaline would provide important information for evaluating the effect of CPAP treatment.     

The acute effects of continuous positive airway pressure and oxygen administration on blood pressure during obstructive sleep apnea.

We have measured blood pressure continuously with a digital artery blood pressure monitor in eight patients with severe obstructive sleep apnea (OSA) during 30 min each of wakefulness, OSA, OSA with added oxygen to keep saturation above 96 percent at all times (OSA+O2), and nasal continuous positive airway pressure (CPAP) therapy. Mean blood pressures were not different between wakefulness, OSA, OSA+O2, and CPAP, although the variability in blood pressure was significantly greater during OSA and OSA+O2 than during wakefulness and CPAP. The addition of oxygen did not attenuate the variability in blood pressure. Using multiple linear regression modeling to further dissect out the principal variables determining the postapneic blood pressure rise, we found that only apnea length (r2 = 0.28, p less than 0.0001) and pulse rate changes (r2 = 0.15, p less than 0.0001) remained significantly related to SBPmax, while hypoxemia did not. We found the same trends in the other variables SBPten, DBPmax, and DBPten. Hypoxemia made a small contribution to the size of DBPmax, although this was small by comparison with apnea length. We conclude that CPAP treatment of OSA does not lower mean blood pressure acutely, although it significantly reduces the large oscillations in blood pressure seen in patients with untreated OSA. The rise in blood pressure following each apnea is not primarily due to arterial desaturation but is related to apnea length and may be caused by increased sympathetic activity secondary to arousal.     

持续气道正压通气对于阻塞性睡眠呼吸暂停相关性高血压的治疗效果研究进展

阻塞性睡眠呼吸暂停常影响睡眠质量并引起心血管疾病,其中高血压发病率最高。目前对于阻塞性睡眠呼吸暂停与高血压之间的关系及机制仍在探索中,而持续气道正压通气作为阻塞性睡眠呼吸暂停的有效治疗方法,对于血压的降压作用说法不一。了解阻塞性睡眠呼吸暂停与高血压之间的关系机制及持续气道正压通气的治疗效果,将有助于更好的临床实践。     

Transtracheal oxygen, nasal CPAP and nasal oxygen in five patients with obstructive sleep apnea.

The effect of transtracheal oxygen administration by means of a 9-French (2.7 mm) percutaneous catheter was assessed in five patients with severe obstructive sleep apnea. We hypothesized that the delivery of oxygen below the site of airway obstruction should reduce the arterial oxygen desaturation during apneas and hypopneas, thereby increasing respiratory stability. Standard sleep and respiratory measurements were recorded in these subjects with all-night polysomnography on nonconsecutive nights during four experimental conditions: room air (BL), nasal continuous positive airway pressure (CPAP), nasal O2 (NC O2), and transtracheal O2 (TT O2). In three of these subjects, room air was infused (TT RA) at flow rates comparable to TT O2. Compared with baseline room air measurements, TT O2 not only significantly increased the SaO2 nadir from 70.4 percent to 89.7 percent (p less than 0.01), but it also reduced the frequency of sleep apnea/hypopnea from 64.6 to 26.2/h sleep (p less than 0.01). NC O2 ameliorated desaturation during apnea/hypopnea (mean SaO2 nadir, 86.2 percent; p less than .01) but did not significantly alter frequency (59.0/h sleep). Nasal CPAP was the most effective means of reducing sleep apnea/hypopnea (13.8/h sleep) but did not abolish desaturations when apneas occurred (mean SaO2 nadir, 80.0 percent). Compared with oxygen, transtracheal infusion of room air appeared to be somewhat effective; however, the small number of studies with TT RA precluded statistical analysis. We believe that TT O2 is superior to NC O2 for some patients with obstructive sleep apnea because continuous oxygen flow below the site of airway obstruction more reliably prevents alveolar hypoxia and respiration is stabilized. Infusion of air or oxygen through the tracheal catheter flow may also increase mean airway pressure and reduce obstructive apnea similar to nasal CPAP. We conclude that TT O2 may be an effective alternative mode of therapy for some patients with severe sleep apnea/hypopnea when nasal CPAP is not tolerated or when combined oxygen and nasal CPAP are required.     

Proportional positive airway pressure: a new concept to treat obstructive sleep apnoea.

Proportional positive airway pressure (PPAP) was designed to optimize airway pressure for the therapy of obstructive sleep apnoea (OSA). In a randomized crossover prospective study, the clinical feasibility of PPAP and its immediate effects on the breathing disorder and sleep in comparison with continuous positive airway pressure (CPAP) was evaluated. Twelve patients requiring CPAP therapy underwent CPAP and PPAP titration in a random order. Obstructive and mixed respiratory events could be completely abolished with both forms of treatment. This efficacy could be achieved at a significantly lower mean mask pressure during PPAP titration (8.45+/-2.42 cmH2O) compared to CPAP (9.96+/-2.7 cmH2O) (p=0.002). The mean minimal arterial oxygen saturation (Sa,O2) (82.8+/-6.5%) on the diagnostic night increased significantly (p<0.001) to an average Sa,O2 of 93.35+/-1.71% and 93.19+/-2.9% during CPAP and PPAP titration. Total sleep time, slow wave sleep and rapid eye movement (REM) sleep increased significantly by the same amount during both CPAP and PPAP titration (p<0.001), while sleep stage nonrapid eye movement (NREM) 1 and 2 decreased. Six patients preferred the PPAP titration night, four patients did not have a preference, and two patients preferred CPAP. The present data show that proportional positive airway pressure is as effective as continuous positive airway pressure in eliminating obstructive events and has the same immediate effect on sleep. The lower average mask pressure during proportional positive airway pressure implies potential advantages compared to continuous positive airway pressure. Proportional positive airway pressure presents a new effective therapeutic approach to obstructive sleep apnoea.     

Kardiale Auswirkungen der obstruktiven Schlafapnoe

Sleep disordered breathing, especially obstructive sleep apnea, are common in cardiovascular disease. Negative hemodynamic effects are mediated by nocturnal ischemia and intrathoracal pressure swings. Therefore “therapy resistant” arterial hypertension and congestive heart failure, as well as atrial fibrillation or sleep associated bradycardia are suggestive of sleep disordered breathing. Further on, clinical course of coronary artery disease seems to be influenced by nocturnal breathing disorders. Application of continuous positive airway pressure (CPAP) is effective in most of the patients and attenuates cardiodepressive hemodynamic effects of obstructive sleep apnea.     

Resistant hypertension, obesity, sleep apnea, and aldosterone: theory and therapy

Hypertension resistant to 2 antihypertensive drugs is more common among obese patients than among lean patients. The case we describe and the observations we report suggest that refractoriness among obese hypertensives is frequently caused by obstructive sleep apnea and/or inappropriately high plasma aldosterone levels. In other words, obese hypertensives may have sleep apnea, obese hypertensives without sleep apnea may have inappropriately elevated levels of plasma aldosterone, and a surprising number of obese patients with sleep apnea also have elevated levels of aldosterone. The mechanisms by which obesity and obstructive sleep apnea increase aldosterone levels and raise blood pressure are not understood, but sympathetic nervous system activation and production of nonclassical adrenal stimuli are two possibilities. Obstructive sleep apnea can be detected with a careful history and various sleep studies. Inappropriately elevated aldosterone levels can be detected by measuring the ratio of plasma aldosterone concentration to plasma renin activity. Successful treatment of these resistant hypertensives often can be achieved by devices that provide positive pressure to the upper airway to correct obstructive sleep apnea and by incorporating an aldosterone antagonist in the therapeutic regimen.     

Myocardial perfusion by myocardial contrast echocardiography and endothelial dysfunction in obstructive sleep apnea

Obstructive sleep apnea is associated with increased cardiovascular morbidity and mortality. We investigated myocardial perfusion using real-time quantitative myocardial contrast echocardiography with concurrent assessment of macrovascular and microvascular endothelial dysfunction in normotensive subjects with moderate-to-severe obstructive sleep apnea, who were compared with hypertensive and healthy subjects, as well as the impact of continuous positive airway pressure treatment on obstructive sleep apnea subjects. We measured flow (hyperemia)-mediated dilation and response to glyceryl trinitrate of brachial artery (ultrasound), cutaneous perfusion responses to acetylcholine and sodium nitroprusside (laser Doppler), pulse wave velocity, and circulating endothelial and endothelial progenitor cells in a total of 108 subjects (n=36 each of matched obstructive sleep apnea, hypertension, and healthy cohorts). Subjects with obstructive sleep apnea and hypertension demonstrated abnormal myocardial perfusion (P<0.001 for both comparisons), attenuated brachial artery reactivity (P<0.001), and cutaneous perfusion responses (P<0.001) compared with healthy individuals. Both hypertensive and obstructive sleep apnea patients showed significant improvements in myocardial perfusion (P<0.01), brachial artery reactivity (P<0.001), and cutaneous perfusion responses (P<0.001) after 26 weeks of continuous positive airway pressure therapy. There were no significant differences in pulse wave velocity and endothelial cells across the 3 groups. Concomitant endothelial dysfunction and impaired myocardial perfusion are present in otherwise normal subjects with moderate-to-severe obstructive sleep apnea, and effective continuous positive airway pressure treatment reverses many of these macrovascular/microvascular abnormalities.     

持续正压通气辅助治疗高血压并发睡眠呼吸暂停综合征的临床研究

目的探讨持续正压通气辅助治疗高血压并发睡眠呼吸暂停综合征（SAS）对血压的影响。方法41例高血压并发睡眠呼吸暂停综合征病人,随机分为常规组（21例）和持续正压通气治疗组（20例）均给予常规降压药物治疗4周,治疗在常规治疗基础上加用气道持续正压通气治疗,观察两组治疗前后24 h血压变化。结果治疗组治疗后24 h平均收缩压、舒张压进一步降低,夜间收缩压及舒张压则显著降低（P〈0.01）。结论高血压并发睡眠呼吸暂停综合征病人,在常规应用降压药物同时应用持续正压通气辅助治疗血压下降更理想。     

CPAP治疗重度OSAHS的疗效观察

目的 观察持续气道正压通气(CPAP)治疗重度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的疗效、影响因素.方法 36例确诊为重度OSAHS的患者经CPAP治疗后,观察其治疗前后的呼吸暂停低通气指数(AHI)、夜间最低血氧饱和度(SaO2)及临床症状的变化.结果 治疗后AHI明显下降,夜间最低SaO2及临床症状明显改善.结论 CPAP是治疗重度OSAHS的有效方法.患者的依从性对重度OSAHS的治疗有决定性的意义.     

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。     

Chronic snoring and obstructive sleep apnea syndrome in children

Increased upper airway resistance during sleep may lead to heavy snoring and/or obstructive sleep apnea in infants and children. Clinical symptoms will be seen with increased upper airway resistance during sleep, even without obstructive sleep apnea or significant oxygen saturation drop. It may be responsible for apparent life threatening events (ALTE). Mild cranio-facial morphometric changes are often associated with increased upper airway resistance during sleep, and there is a continuous interaction between airway patency during sleep and maxillo-mandibular growth. Nasal CPAP can be as much a diagnostic tool as a treatment procedure. Orthodontic and surgical approaches may also be combined in the treatment of this significant health problem.