高原红细胞增多症患者夜间睡眠呼吸变化

高原睡眠结构紊乱和周期性呼吸已有较多记载,我们对海拔3730m处8例高原红细胞增多症(HAPC)患者在高原和平原夜间睡眠呼吸变化进行了研究,以探讨高原与平原对其夜间睡眠、呼吸和血氧饱和度(Sao_2)的影响。     

高原睡眠呼吸紊乱与急性高原病的相关性研究进展

高原低氧环境严重影响人的睡眠质量及结构、睡眠呼吸紊乱进一步参与急慢性高原病的发生、发展。急进高原及高原习服人群表现出不同的睡眠呼吸结构的改变,世居藏族人群在高原环境下有良好的睡眠结构和质量。文章通过周期性呼吸、低氧通气反应、引起中枢性睡眠呼吸暂停的环路增益、细胞因子水平和神经递质等方面阐述了高原自然环境中引起睡眠呼吸改变的机制及其与急性高原病发生、发展的相关性,为更好地预防和治疗急性高原病提供新的思路。     

心肺功能运动试验用于急性高山病的评价

为了进一步探讨急性高山病(AMS)的生理学评价指标,先对15名男性健康青年在海拔2261及3417m处进行心肺功能运动试验.结果观察到低氧通气及心搏反应以及动脉血氧饱和度(Sao_2)变化出现较早且敏感。随后对90名男性进入海拔4520m及攀登5620m过程中发生AMS时进行症状学调查,并证实静息动脉血氧分压(Pao_2)和肺泡一动脉氧阶差(AaDO_2)大小与AMS严重程度关系密切。在运动负荷(Vo_(2submax))时,测定静息及运动时最大心率差值(HRD)、动脉二氧化碳分压差值(Paco_2D)及动脉血氧饱和度差值(Sao_2D),由此求得HRD/Sao_2D及Paco_2D/Sao_2D两项指标,分别反映低氧心搏及通气反应能力。对AMS的判别具有敏感性,与以症状学判别相比,总吻合率达92.2％。     

90例原发性癫痫患者睡眠呼吸障碍及其相关事件分析

目的:探讨原发性癫痫患者夜间睡眠呼吸障碍及相关事件的特点.方法:对90例原发性癫痫患者进行夜间多导睡眠图(PSG)检查.分析夜间睡眠呼吸暂停低通气指数、睡眠各期SPO2值及相关腿动事件.结果:本组病人的PSG检测结果表现为SPO2监测显示有26.67%的患者合并有睡眠呼吸暂停低通气综合症(SAHS),合并SAHS组与不合并SAHS组在年龄、体重指数、是否合并高血压病方面进行比较P均<0.05,其差异有统计学意义.两组在病程、性别、发作形式、有无痫样放电、有无周期性腿动方面比较P值均>0.05,其差异无统计学意义.SPO2仪显示癫痫患者夜间存在不同程度低氧事件,其中SPO2最低值均发生在REM期.肌电显示孤立性腿动指数增加人数为27例(占30%),周期性腿动指数增加人数为15人(占16.67%),其中因激醒事件及呼吸事件因素而导致腿动指数增加分别占一定比例,且腿动事件主要集中在NREM期.结论:原发性癫痫患者常伴有睡眠呼吸障碍及夜间低氧事件.     

高原低氧对喜马拉雅旱獭、高原鼠兔、缺氧敏感大鼠颈动脉体超微结构的影响

应用扫描电镜结合透射电镜技术,对上海(海拔10米)的大鼠,5天内从上海急进到海拔3300米的大鼠,由北京引入西宁的子4代大鼠,同高原的喜马拉雅旱獭和高原鼠兔的颈动脉体微细结构进行对比观察。结果表明,高原低氧环境使由低海拔急进到高海拔的大鼠颈动脉体Ⅰ型细胞增生、肿胀、体积增大,胞浆中致密核心囊泡数量减少,线粒体变性肿胀,神经末稍中突触囊泡减少,Ⅰ型细胞表面微绒毛变性脱落;而喜马拉雅旱獭和高原鼠兔对高原低氧环境有较好的适应,未见缺氧损害征象。     

不同缺氧模式对青年男性睡眠结构的影响*

目的:本研究通过对正常人群与呼吸暂停综合症人群在不同海拔高度低氧环境下睡眠结构的分析,探讨人体内源性摄氧受限与外源性环境缺氧两个不同缺氧因素导致人体睡眠结构的差异。方法:通过匹兹堡睡眠质量指数量表筛查16名不存在睡眠问题的男性青年,在常氧环境中测得其睡眠过程中的呼吸暂停低通气指数(AHI),并根据AHI将其分为正常组(NOR组,n=8)和呼吸暂停综合征组(OSA组,n=8)。本研究采用吸入低O₂混合气的方法模拟不同海拔高度,受试者在每次测试中连续吸入10 h低O₂混合气进行模拟高海拔环境下睡眠测试。在平原环境下测试的一周进行后O₂浓度为16.3%(模拟海拔2 000 m)的常压低氧环境下进行睡眠测试,两周后进行O₂浓度为12.7%(模拟海拔4 000 m)的常压低氧环境下进行睡眠测试。结果:随着海拔高度上升,受试者睡眠过程中的REM期睡眠占比从平原时的12.03%降至模拟海拔2 000 m时的9.33%、模拟海拔4 000 m时7.15%(P＜0.05),但不同海拔高度下睡眠过程中的浅睡眠和深睡眠占比均无显著性变化(P＞0.05)。NOR组和OSA组的睡眠效率分别是82%、69.5%(P＜0.01),睡眠过程中的REM期占比分别是7.56%、11.2%(P＜0.05);深睡眠占比分别是30.26%、 19.13%(P＜0.01)。但NOR组和OSA组睡眠过程中的浅睡眠占比无明显差异(P＞0.05)。结论:与海拔高度上升导致的外源性缺氧相比,OSA引起的内源性缺氧还将影响青年男性睡眠过程中的深睡眠和睡眠效率。且轻度的阻塞性呼吸暂停综合征患者急性暴露在低氧环境下睡眠过程中具有更强的低氧耐受性。     

周期性呼吸的研究进展

周期性呼吸是一种异常的呼吸模式,可引起频繁的觉醒,使睡眠结构片段化,导致睡眠质量下降,严重影响人们的身体健康。周期性呼吸产生的主要机制是负反馈调节,其类型可分为生理性(婴幼儿及儿童、健康人运动后等)和病理性(心力衰竭患者、进入高海拔地区和药物相关性中枢性睡眠呼吸暂停)。目前对于周期性呼吸的病因、形成机制及治疗方面还存在较多争议,本研究主要从周期性呼吸的形成机制、分类及治疗等方面的进展进行综述。     

高原低氧对高原鼠兔和大白鼠肺泡Ⅱ型细胞及表面活性物质超微结构的影响

本文报道高原低氧(海拔3300米)对高原鼠兔、移居高原大鼠、急进高原大鼠的肺泡Ⅱ型细胞及表面活性物质超微结构的影响。发现高原鼠兔肺占体重的百分比低于移居高原大鼠(P>0.05)和急进高原大鼠(P<0.001)。透射电镜和扫描电镜观察,表明急进高原大鼠肺泡Ⅱ型细胞微绒毛减少,线粒体变性肿胀,板层体排空、合成减少。而高原鼠兔未出现上述超微结构改变。移居高原大鼠的微细结构变化介乎于高原鼠兔与急进高原大鼠之间。     

悬雍垂腭咽成形术治疗阻塞性睡眠呼吸暂停综合征的护理

阻塞性睡眠呼吸暂停综合征（OSAHS）是由于上气道口咽部阻塞,频发睡眠呼吸暂停、通气不良,引起低氧血症及高碳酸血症,使机体产生一系列病理生理改变的临床综合征。     

模拟高海拔低氧对人体睡眠的影响

在模拟不同海拔高度的低氧条件暴露下,我们记录和测定了6名对象的睡眠生理各项指标。结果如下:在急性低氧暴露下所有对象均出现了睡眠障碍,主要是在夜间规定睡眠时间中觉醒期和觉醒次数增加,深睡眠期和快眼动期减少,睡眠各期的呼吸频率和心率增加。随着低氧暴露时间的延长和多次空气潜水后,各睡眠生理指标有向海平对照值水平发展的趋势。4500m以上的低氧暴露下,所有对象在睡眠中都有周期性呼吸现象出现,并影响体内的缺氧。     

Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude.

We examined the initial effect of sleeping at a simulated moderate altitude of 2,650 m on the frequency of apneas and hypopneas, as well as on the heart rate and blood oxygen saturation from pulse oximetry (SpO2) during rapid eye movement (REM) and non-rapid eye movement (NREM) sleep of 17 trained cyclists. Pulse oximetry revealed that sleeping at simulated altitude significantly increased heart rate (3 +/- 1 beats/min; means +/- SE) and decreased SpO2 (-6 +/- 1%) compared with baseline data collected near sea level. In response to simulated altitude, 15 of the 17 subjects increased the combined frequency of apneas plus hypopneas from baseline levels. On exposure to simulated altitude, the increase in apnea was significant from baseline for both sleep states (2.0 +/- 1.3 events/h for REM, 9.9 +/- 6.2 events/h for NREM), but the difference between the two states was not significantly different. Hypopnea frequency was significantly elevated from baseline to simulated altitude exposure in both sleep states, and under hypoxic conditions it was greater in REM than in NREM sleep (7.9 +/- 1.8 vs. 4.2 +/- 1.3 events/h, respectively). Periodic breathing episodes during sleep were identified in four subjects, making this the first study to show periodic breathing in healthy adults at a level of hypoxia equivalent to 2,650-m altitude. These results indicate that simulated moderate hypoxia of a level typically chosen by coaches and elite athletes for simulated altitude programs can cause substantial respiratory events during sleep.     

Nocturnal periodic breathing at altitudes of 6,300 and 8,050 m

Nocturnal periodic breathing was studied in eight well-acclimatized subjects living at an altitude of 6,300 m [barometric pressure (PB) 350-352 Torr] for 3-5 wk and in four subjects during one night at 8,050 m altitude (PB 281-285 Torr). The measurements at 6,300 m included tidal volume by inductance plethysmography, arterial O2 saturation by ear oximetry (calibrated by arterial blood samples), electrocardiogram (ECG), and electrooculogram. At 8,050 m, periodic breathing was inferred from the cyclical variation in heart rate obtained from a night-long ECG record. All subjects at 6,300 m altitude showed well-marked periodic breathing with apneic periods. Cycle length averaged 20.5 s with 7.9 s apnea. Minimal arterial O2 saturation averaged 63.4% corresponding to a PO2 of approximately 33 Torr, i.e., approximately 6 Torr lower than the normal value at rest during daytime. This was probably the most severe hypoxemia of the 24-h period. At 8,050 m altitude, the cycle length averaged 15.4 s, much longer than predicted by a theoretical model. Cyclical variations in heart rate caused by periodic breathing occurred in all subjects, but abnormal cardiac rhythms such as ventricular premature contractions were uncommon. The severe arterial hypoxemia caused by periodic breathing may be an important determinant of tolerance to these great altitudes.     

Alterations in cerebral dynamics at high altitude following partial acclimatization in humans: wakefulness and sleep.

We tested the hypothesis that, following exposure to high altitude, cerebrovascular reactivity to CO2 and cerebral autoregulation would be attenuated. Such alterations may predispose to central sleep apnea at high altitude by promoting changes in brain PCO2 and thus breathing stability. We measured middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound) and arterial blood pressure during wakefulness in conditions of eucapnia (room air), hypocapnia (voluntary hyperventilation), and hypercapnia (isooxic rebeathing), and also during non-rapid eye movement (stage 2) sleep at low altitude (1,400 m) and at high altitude (3,840 m) in five individuals. At each altitude, sleep was studied using full polysomnography, and resting arterial blood gases were obtained. During wakefulness and polysomnographic-monitored sleep, dynamic cerebral autoregulation and steady-state changes in MCAv in relation to changes in blood pressure were evaluated using transfer function analysis. High altitude was associated with an increase in central sleep apnea index (0.2 +/- 0.4 to 20.7 +/- 23.2 per hour) and an increase in mean blood pressure and cerebrovascular resistance during wakefulness and sleep. MCAv was unchanged during wakefulness, whereas there was a greater decrease during sleep at high altitude compared with low altitude (-9.1 +/- 1.7 vs. -4.8 +/- 0.7 cm/s; P < 0.05). At high altitude, compared with low altitude, the cerebrovascular reactivity to CO2 in the hypercapnic range was unchanged (5.5 +/- 0.7 vs. 5.3 +/- 0.7%/mmHg; P = 0.06), while it was lowered in the hypocapnic range (3.1 +/- 0.7 vs. 1.9 +/- 0.6%/mmHg; P < 0.05). Dynamic cerebral autoregulation was further reduced during sleep (P < 0.05 vs. low altitude). Lowered cerebrovascular reactivity to CO2 and reduction in both dynamic cerebral autoregulation and MCAv during sleep at high altitude may be factors in the pathogenesis of breathing instability.     

Metabolic consequences of reduced frequency breathing during submaximal exercise at moderate altitude

The intention of this study was to determine the metabolic consequences of reduced frequency breathing (RFB) at total lung capacity (TLC) in competitive cyclists during submaximal exercise at moderate altitude (1520 m; barometric pressure, PB = 84.6 kPa; 635 mm Hg). Nine trained males performed an RFB exercise test (10 breaths.min-1) and a normal breathing exercise test at 75-85% of the ventilatory threshold intensity for 6 min on separate days. RFB exercise induced significant (P less than 0.05) decreases in ventilation (VE), carbon dioxide production (VCO2), respiratory exchange ratio (RER), ventilatory equivalent for O2 consumption (VE/VO2), arterial O2 saturation and increases in heart rate and venous lactate concentration, while maintaining a similar O2 consumption (VO2). During recovery from RFB exercise (spontaneous breathing) a significant (P less than 0.05) decreases in blood pH was detected along with increases in VE, VO2, VCO2, RER, and venous partial pressure of carbon dioxide. The results indicate that voluntary hypoventilation at TLC, during submaximal cycling exercise at moderate altitude, elicits systemic hypercapnia, arterial hypoxemia, tissue hypoxia and acidosis. These data suggest that RFB exercise at moderate altitude causes an increase in energy production from glycolytic pathways above that which occurs with normal breathing.     

Plasma adenosine and hypoxemia in patients with sleep apnea

Severe hypoxemia causes ATP depletion and increased adenosine production in many body tissues. Therefore we hypothesized that patients with sleep apnea and severe hypoxemia during sleep have higher adenosine production and higher plasma adenosine levels than patients without hypoxemia. Twelve patients with sleep apnea and six normal volunteers had plasma adenosine levels measured by high-performance liquid chromatography. Each patient with sleep apnea had a polysomnograph sleep study with oxyhemoglobin saturation continuously recorded. Five of 12 patients with sleep apnea had both sleep apnea and severe hypoxemia during sleep. These patients with severe nocturnal hypoxemia had significantly higher plasma adenosine levels (means +/- SD 9.7 +/- 5.5 X 10(-8) M) than either a group of six normal volunteers (3.5 +/- 0.7 X 10(-8) M) or a group of seven patients with sleep apnea without hypoxemia at night (3.1 +/- 1.5 X 10(-8) M) (P less than 0.01). In addition plasma adenosine levels were significantly correlated with two indexes of nocturnal hypoxemia (desaturation index rs = 0.79, and median oxyhemoglobin saturation during sleep rs = -0.75, P less than 0.01). Plasma adenosine markedly fell to a normal level in the only two patients with sleep apnea who had successful treatment of their multiple apneas and accompanying severe hypoxemia during sleep.     

Carotid body denervation eliminates apnea in response to transient hypocapnia.

We determined the effects on breathing of transient ventilatory overshoots and concomitant hypocapnia, as produced by pressure support mechanical ventilation (PSV), in intact and carotid body chemoreceptor denervated (CBX) sleeping dogs. In the intact dog, PSV-induced transient increases in tidal volume and hypocapnia caused apnea within 10-11 s, followed by repetitive two-breath clusters separated by apneas, i.e., periodic breathing (PB). After CBX, significant expiratory time prolongation did not occur until after 30 s of PSV-induced hypocapnia, and PB never occurred. Average apneas of 8.4 +/- 1-s duration after a ventilatory overshoot required a decrease below eupnea of end-tidal Pco(2) 5.1 +/- 0.4 Torr below eupnea in the intact animal and 10.1 +/- 2 Torr in the CBX dog, where the former reflected peripheral and the latter central dynamic CO(2) chemoresponsiveness, as tested in the absence of peripheral chemoreceptor input. Hyperoxia when the dogs were intact shortened PSV-induced apneas and reduced PB but did not mimic the effects of CBX. We conclude that, during non-rapid eye movement sleep, carotid chemoreceptors are required to produce apneas that normally occur after a transient ventilatory overshoot and for PB.     

Sleep problems in individuals with 11q terminal deletion disorder (Jacobsen syndrome)

Characteristics of sleep and sleep problems were investigated in 43 individuals with 11q terminal deletion disorder (Jacobsen syndrome). Data were collected using a sleep questionnaire. Ten individuals (23%) had a sleep problem. Settling problems, frequent night waking and early waking occurred in 2 (4%), 7 (16%) and 2 (6%) individuals, respectively. Twenty-two individuals (54%) had a history of sleep problems. Twenty-five individuals (60%) showed restless sleep and 23 individuals (54%) slept in an unusual position. Apart from frequent coughs, no significant relationships were found between the presence of a sleep problem and other variables, such as age, level of ID, breathing problems, heart defects, constipation, daytime activity and behavioral diagnosis, restless sleep and sleeping in an unusual positions.     

Voluntary breath holding in the obese

Alveolar gas tensions and arterial O2 saturation (Sao2) during a voluntary breath hold at functional residual capacity (FRC) were examined in 13 healthy seated subjects. An excellent correlation (r = 0.80) was found between the fall of alveolar O2 tensions (delta PETo2) and body weight, expressed as the ratio of weight to height (wt/ht, kg/cm). An even greater correlation (r = 0.89) was found between delta PETo2 and the ratio of breath-hold time X O2 consumption/FRC. Alveolar Po2 decreased to 70 mmHg in the obese group after just 15 s of apnea, whereas this degree of hypoxia did not occur in the nonobese until the breath hold was sustained for 30 s. This variable rate of fall of alveolar Po2 during a breath hold can be ascribed to the changes of O2 consumption (Vo2) and FRC associated with changing body weight. In the obese, Vo2/FRC was twice as large as in the nonobese, thus accounting for the differences of breath-hold time needed to obtain the same alveolar Po2. Sao2 measured at the end of the breath hold was the same as that value predicted from the reduction of PETo2. This suggests that the fall of alveolar Po2 can entirely account for the observed fall of O2 saturation and that venous admixture had not increased during the 15-s apnea. In patients with sleep apnea, the ratio of Vo2/(initial lung volume) may also be an important determinant of the severity of hypoxemia observed.     

Waking and genioglossus muscle responses to upper airway pressure oscillation in sleeping dogs

We studied waking and genioglossus electromyographic (EMGgg) responses to oscillating pressure waves applied to the upper airways of three sleeping dogs. The dogs were previously prepared with a permanent side-hole tracheal stoma and were trained to sleep with a tight-fitting snout mask, hermetically sealed in place, while breathing through a cuffed endotracheal tube inserted through the tracheostomy. Sleep state was determined by behavioral, electroencephalographic, and electromyographic criteria, and EMGgg activity was measured using fine bipolar electrodes inserted directly into the muscle. Oscillatory pressure waves of 30 Hz and +/- 3 cmH2O (tested at atmospheric and subatmospheric upper airway pressures) were applied at the dog's nostrils or larynx, either constantly for a period of 1 min or in 0.5-s bursts. We found that the pressure stimulus had two major effects. First, it was a potentially powerful arousal-promoting stimulus. Arousal occurred in 78% of tests in slow-wave sleep (SWS) and 55% of tests in rapid-eye-movement (REM) sleep, with swallowing and sighing accompanying many of the arousals. Second, it produced an immediate and sustained augmentation of EMGgg, in wakefulness, SWS, and REM sleep. We conclude that oscillatory pressure waves in the upper airway, as found in snoring, produce reflex responses that help maintain upper airway patency during sleep. Loss of this type of reflex might contribute to the onset of obstructive sleep apnea in chronic snorers.