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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

15 patients with obstructive sleep apnea syndrome and arterial hypertension (H-OSAS), 25 normotensive patients with sleep apnea syndrome (N-OSAS) and 20 healthy age-matched controls (C) were included in this study. Ventilatory responses to activation (hypoxia) and inactivation (hyperoxia) of carotid chemoreceptors were studied in all subjects. Relationship between hypoxic ventilatory reactivity and nocturnal bradycardia during apnea-phases was analysed in both groups of patients. Results and conclusions. 1. We found an impairment of ventilatory response to hypoxia in H-OSAS and N-OSAS patients. However, the increase in ventilation in response to hypoxia was significantly greater in H-OSAS as compared to N-OSAS patients. 2. An augmented ventilatory response to inactivation of carotid chemoreceptors (the decrease in ventilation), observed in H-OSAS patients, indicates an increase in resting peripheral chemoreceptors drive in this group of patients. 3. The relationship between ventilatory response to hypoxia and nocturnal bradycaria in obstructive sleep apnea patients suggests, that hypoxic reactivity of arterial chemoreceptors might be involved in the origin of bradycardia during apnea events.
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PMID:Peripheral chemoreceptor reflex in obstructive sleep apnea patients; a relationship between ventilatory response to hypoxia and nocturnal bradycardia during apnea events. 186 15

Sleep apnea and other respiratory diseases produce hypoxemia and hypercapnia, factors that adversely affect skeletal muscle performance. To examine the effects of these chemical alterations on force production by an upper airway dilator muscle, the contractile and endurance characteristics of the geniohyoid muscle were examined in situ during severe hypoxia (arterial PO2 less than 40 Torr), mild hypoxia (PO2 45-65 Torr), and hypercapnia (PCO2 55-80 Torr) and compared with hyperoxic-normocapnic conditions in anesthetized cats. Muscles were studied at optimal length, and contractile force was assessed in response to supramaximal electrical stimulation of the hypoglossal nerve (n = 7 cats) or geniohyoid muscle (n = 2 cats). There were no significant changes in the twitch kinetics or force-frequency curve of the geniohyoid muscle during hypoxia or hypercapnia. However, the endurance of the geniohyoid, as reflected in the fatigue index (ratio of force at 2 min to initial force in response to 40-Hz stimulation at a duty cycle 0.33), was significantly reduced by severe hypoxia but not by hypercapnia or mild hypoxia. In addition, the downward shift in the force-frequency curve after the repetitive stimulation protocol was greater during hypoxia than hyperoxia, especially at higher frequencies. In conclusion, the ability of the geniohyoid muscle to maintain force output during high levels of activation is adversely affected by severe hypoxia but not mild hypoxia or hypercapnia. However, none of these chemical perturbations affected muscle contractility acutely.
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PMID:Effects of hypoxia and hypercapnia on geniohyoid contractility and endurance. 193 46

We studied the effects of hyperoxia and hypercapnia on obstructive apneic episodes (OAE) in a 39-year-old male with the sleep apnea and hypersomnolence syndrome (SAHS). While inspiring room air, our patient spent approximately 50% of his non-REM sleep time in OAE. When the inspired gas was changed to 100% oxygen, the frequency of the OAE decreased slightly, but a statistically significant increase in the duration of each episode was noted. Additionally, a CO2 rebreathe under hyperoxic conditions was carried out during non-REM sleep; no OAE were noted during this rebreathe. Therefore, this latter observation suggests that hypercapnia under hyperoxic conditions may reduce the frequency of OAE in patients with the SAHS.
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PMID:Effects of respiratory gases on the frequency and duration of obstructive apneic episodes in a patient with the sleep apnea-hypersomnolence syndrome. 680 21

Eight adult patients with sleep apnea were studied to evaluate the ventilatory and cardiac effects of hyperoxia on an acute basis. Five patients then used low-flow nighttime oxygen for 30 to 90 days. The results of the acute study showed that for 30-min study periods, the total number of apneas and per cent apnea time (duration of apneas divided by sleep time) decreased significantly from the room air to the oxygen period (207 to 68, p less than 0.05; 41.1 +/- 18.3% SD to 20.5 +/- 14.4%, p less than 0.05, respectively). Also, the apnea-associated slowing in heart rate is blocked by the supplemental oxygen. Three patients receiving oxygen at home decreased their per cent apnea time by greater than 60%. These patients also responded to the acute administration of hyperoxia by a decrease in apnea time greater than 60%. One patient prolonged the apnea time, and one had a minimal positive response, both again reflecting their acute studies. These data suggested that the severe hypoxemia that develops during an apnea in this syndrome has a central ventilatory effect that propagates the apneas and is significantly reversed by hyperoxia.
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PMID:Acute and long-term ventilatory effects of hyperoxia in the adult sleep apnea syndrome. 706 20

To determine the characteristics of and mechanisms causing the bradycardia during sleep apnea (SA), both patients with SA and normals were studied. Evaluation of six consecutive SA patients demonstrated that bradycardia occurred during 95% of all apneas (central, obstructive, and mixed) and became marked with increased apnea length (P less than 0.01) and increased oxyhemoglobin desaturation (P less than 0.01). Heart rate slowed 9.5 beats per minute (bpm) during apneas of 10-19 s in duration, 11.4 bpm during 20-39s apneas, and 16.6 bpm during 40-59-s apneas. Sleep stage had no effect unexplained by apnea length or degree of desaturation. Oxygen administration to four SA patients completely prevented the bradycardia although apneas lengthened (P less than 0.05) in three. Sleeping normal subjects did not develop bradycardia during hypoxic hyperpnea but, instead, HR increased with hypoxia in all sleep stages, although the increase in HR was not as great as that which occurred while awake. Breath holding in awake normals did not result in bradycardia during hyperoxia (SaO2 = 99%), but was consistently (P less than 0.01) associated with heart rate slowing during room air breath-holds (-6 bpm) at SaO2 = 93%, with more striking slowing (-20 bpm) during hypoxic breath-holds (P less than 0.01) at SaO2 = 78%. Breath holding during hyperoxic hypercapnia had no significant effect on rate. Breath holding in awake SA subjects demonstrated similar findings. We conclude that the bradycardia of SA is a consistent feature of apnea and results from the combined effect of cessation of breathing plus hypoxemia.
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PMID:Bradycardia during sleep apnea. Characteristics and mechanism. 708 75

Oscillations of arterial pressure during sleep are the hemodynamic hallmark of the sleep apnea syndrome. The mechanism of these transient pressure elevations is incompletely understood. To investigate the role of the arterial chemoreflex in the neurocirculatory responses to apnea, we measured mean arterial pressure (MAP; Finapres) and muscle sympathetic nerve activity (MSNA; peroneal microneurography) during voluntary end-expiratory apnea during exposure to room air, 10.5% O2 in N2 (hypoxemia), and 100% O2 (hyperoxia) in 11 healthy men. While the men breathed spontaneously, MSNA (in bursts/min) rose during hypoxemia and decreased during hyperoxia and MAP remained unchanged. During room air exposure, apnea led to a rise of 94 +/- 54% in MSNA total amplitude and a rise of 6.5 +/- 2.1 mmHg in MAP. MSNA and MAP increased by 616 +/- 158% and 10.8 +/- 2.4 mmHg, respectively, during hypoxemic apnea of equal duration (time-matched responses) and by 98 +/- 41% and 4.9 +/- 2.0 mmHg, respectively, during hyperoxic apnea (P < 0.05 for hypoxemic vs. hyperoxic apnea for both). Thus, in awake healthy humans, activation of the arterial chemoreflex by hypoxemia appears to contribute importantly to the sympathetic and blood pressure responses to apnea.
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PMID:Sympathetic and blood pressure responses to voluntary apnea are augmented by hypoxemia. 786 56

Sleep apnea occurs in humans and experimental animals. We examined whether it also arises in adult mice. Ventilation in male adult 129/Sv mice was recorded concomitantly by electroencephalograms and electromyograms for 6 h by use of body plethysmography. Apnea was defined as cessation of plethysmographic signals for longer than two respiratory cycles. While mice breathed room air, 32.3 +/- 6.9 (mean +/- SE, n = 5) apneas were observed during sleep but not in quiet awake periods. Sleep apneas were further classified into two types. Postsigh apneas occurred exclusively during slow-wave sleep (SWS), whereas spontaneous apneas arose during both SWS and rapid eye movement sleep. Compared with room air (9.1 +/- 1.4/h of SWS), postsigh apneas were more frequent in hypoxia (13.7 +/- 2.1) and less frequent in hyperoxia (3.6 +/- 1.7) and hypercapnia (2.8 +/- 2.1). Our data indicated that significant sleep apnea occurs in normal adult mice and suggested that the mouse could be a promising experimental model with which to study the genetic and molecular basis of respiratory regulation during sleep.
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PMID:Sleep apnea and effect of chemostimulation on breathing instability in mice. 1243 67

The gas composition of breathing air is a very important stimulus for the control of breathing. The different partial pressures of O2 and CO2 independently trigger individually different reactions (respiratory response), which can be measured as a change of respiratory minute volume. Investigations of the respiratory control in patients with obstructive sleep apnoea (OSA) have up to now been restricted to an analysis of the breathing patterns at night. Therefore we have developed a computer-controlled device which allows a flexible composition of the air to be inhaled using a regulated feet-back circle. With this system it is possible to produce a hypercapnia test as well as a hyperoxia and an isocapnic hypoxia test. The simultaneous recording of all relevant respiratory parameters (AF, AMV, ETCO2, SpO2, FiO2) and the parallel recording of continuous blood pressure allow a quantitative description of the respiratory regulation of patients with OSA with exactly defined tests.
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PMID:[Measuring hypoxic and hypercapnic respiratory response in patients with obstructive sleep apnea]. 1246 25

During development, windows of increased vulnerability to noxious stimulus occur. These critical periods of maturation represent times at which the maturing animal is uniquely susceptible to external perturbations that may alter the ultimate configuration of neural networks and their associated function(s), thereby inducing persistent (mal)adaptive changes. In contrast, when comparable perturbations are applied to adult animals the associated adaptive changes do not typically persist. This principle has been demonstrated in models of respiratory plasticity in developing mammals including exposure to sustained hypoxia, hyperoxia, and pharmacological agents. Recently, intermittent hypoxia (IH) during development has also been implicated as a potent inducer of respiratory plasticity. Altered ventilatory patterning induced by IH is distinct from other stimuli and elicits markedly different responses in the developing mammal as compared to the adult. Furthermore, adaptations to acute IH (AIH) exposure may involve mechanisms that differ from those invoked by chronic IH exposure (CIH). Thus, critical examination of IH exposure paradigms is also an important consideration. Greater understanding of IH-induced ventilatory plasticity, particularly in the developing animal, will undoubtedly increase our understanding of IH related diseases such as sleep disordered breathing, and perhaps provide future directions for intervention strategies.
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PMID:Developmental plasticity of respiratory control following intermittent hypoxia. 1620 18

Although sleep apnoea is very common in patients with end-stage renal disease, the physiological mechanisms for this association have not yet been determined. The current authors hypothesised that altered respiratory chemo-responsiveness may play an important role. In total, 58 patients receiving treatment with chronic dialysis were recruited for overnight polysomnography. A modified Read rebreathing technique, which is used to assess basal ventilation, ventilatory sensitivity and threshold, was completed before and after overnight polysomnography. Patients were divided into apnoeic (n = 38; apnoea/hypopnoea index (AHI) 35+/-22 events.h(-1)) and nonapnoeic (n = 20; AHI 3+/-3 events.h(-1)) groups, with the presence of sleep apnoea defined as an AHI >10 events.h(-1). While basal ventilation and the ventilatory recruitment threshold were similar between groups, ventilatory sensitivity during isoxic hypoxia (partial pressure of oxygen (PO2) 6.65 kPa) and hyperoxia (PO2) 19.95 kPa) was significantly greater in apnoeic patients. Overnight changes in chemoreflex responsiveness were similar between groups. In conclusion, these data indicate that the responsiveness of both the central and peripheral chemoreflexes is augmented in patients with sleep apnoea and end-stage renal disease. Since increased ventilatory sensitivity to hypercapnia destabilises respiratory control, the current authors suggest this contributes to the pathogenesis of sleep apnoea in this patient population.
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PMID:Enhanced chemo-responsiveness in patients with sleep apnoea and end-stage renal disease. 1651 Apr 59


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