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)

Two obese patients with sleep apnea syndrome were administered chlormadinone acetate (CMA), a synthetic progesterone, known as a potent respiratory stimulant to augment load compensation response as well as CO2 chemosensitivity. Before CMA administration, both cases showed normal chemosensitivity of hypoxic and hypercapnic ventilatory responses (HVR and HCVR) at daytime, although marked oxygen desaturation with sleep apnea was observed. During CMA administration for 7 days, HVR, HCVR and occlusion pressure response to flow-resistive loading were altogether augmented. In one case obstructive sleep apnea (OSA) was altered to obstructive hypopnea, and in the other case central apnea disappeared completely, resulting in remarkable improvement of oxygen desaturation at sleep and daytime somnolence in both cases. We conclude that CMA might be useful in the treatment of sleep apnea syndrome.
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PMID:Obese patients with sleep apnea syndrome treated by progesterone. 247 20

We compared the changes in nasal and pharyngeal resistance induced by modifications in the central respiratory drive in 8 patients with sleep apnea syndrome (SAS) with the results of 10 normal men. Upper airway pressures were measured with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other above the uvula. Nasal and pharyngeal resistances were calculated at isoflow. During CO2 rebreathing and during the 2 min after maximal voluntary hyperventilation, we continuously recorded upper airway pressures, airflow, end-tidal CO2, and the mean inspiratory flow (VT/TI); inspiratory pressure generated at 0.1 s after the onset of inspiration (P0.1) was measured every 15-20 s. In both groups upper airway resistance decreased as P0.1 increased during CO2 rebreathing. When P0.1 increased by 500%, pharyngeal resistance decreased to 17.8 +/- 3.1% of base-line values in SAS patients and to 34.9 +/- 3.4% in normal subjects (mean +/- SE). During the posthyperventilation period the VT/TI fell below the base-line level in seven SAS patients and in seven normal subjects. The decrease in VT/TI was accompanied by an increase in upper airway resistance. When the VT/TI decreased by 30% of its base-line level, pharyngeal resistance increased to 319.1 +/- 50.9% in SAS and 138.5 +/- 4.7% in normal subjects (P less than 0.05). We conclude that 1) in SAS patients, as in normal subjects, the activation of upper airway dilators is reflected by indexes that quantify the central inspiratory drive and 2) the pharyngeal patency is more sensitive to the decrease of the central respiratory drive in SAS patients than in normal subjects.
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PMID:Effects of respiratory drive on upper airways in sleep apnea patients and normal subjects. 250 8

Twenty-eight children whose parents reported sleep apnoea were investigated. In 15 infants apnoeic periods during sleep could be confirmed during clinical observation. Ventilatory responses to CO2 were measured in all infants, in 23 during sleep in 5 only when awake. A very wide range of CO2 sensitivities was found. In four children there was no ventilatory response or even a paradox one: a decrease in ventilation as PACO2 was increased. Two of these non-responding children died later, one still sleeps in a respirator aged three, and one developed a normal CO2 sensitivity a few months later. It is concluded that the parent's account of an apnoeic incident during sleep is not always reliable. A ventilatory response to CO2 is a useful tool with which to identify infants at risk of death, possibly related to a defective control of ventilation. The actual value of the CO2 sensitivity hardly gives any useful information, due to the wide range of "normal" reactions. No or negative ventilatory responses to CO2 seem to be indicators of high risk children, and may possibly play a role in SIDS incidents.
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PMID:Ventilatory response to CO2 in infants with alleged sleep apnoea. 308

There is as yet no convincing evidence that acetazolamide, a carbonic anhydrase inhibitor, is effective in obstructive sleep apnoea. A study was therefore designed to examine the effect of acetazolamide (250 mg/day) on sleep events and ventilatory control during wakefulness in nine patients with the sleep apnoea syndrome. In eight of the nine patients the apnoea index and the total duration of apnoea were reduced by acetazolamide, and the mean (SEM) apnoea index of all patients changed from 25.0 (6.7) to 18.1 (5.8) episodes an hour. Furthermore, the total time of arterial oxygen desaturation (SaO2)--more than 4% depression in SaO2 from the baseline sleeping level--divided by total sleep time was also significantly decreased and its mean (SEM) value improved from 24.1 (7.9) to 13.6 (4.8)% of total sleep time. Five of the seven patients with varying degrees of daytime hypersomnolence had their symptoms obviously improved. There was no patient whose predominant type of apnoea was converted from the obstructive to the central type, or vice versa. In the studies of wakefulness, metabolic acidosis, an increase of arterial oxygen tension (PaO2) and a decrease of arterial carbon dioxide tension (PaCO2) were observed. The slopes of the occlusion pressure response and the ventilatory response to carbon dioxide increased, and the carbon dioxide ventilatory response line shifted to the left. It is suggested that acetazolamide cannot remove apnoea completely but has a beneficial effect in mild cases of obstructive sleep apnoea through an augmentation of central (CO2, H+) drive and a stabilising effect on ventilatory control.
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PMID:Effects of acetazolamide in patients with the sleep apnoea syndrome. 312 12

Morbid obesity is not infrequently associated with severe respiratory impairment. In our experience approximately 10 per cent of morbidly obese patients who underwent gastric surgery had severe respiratory impairment. Respiratory insufficiency of obesity can be divided into two primary breathing disorders: the obstructive sleep apnea syndrome (SAS) and the obesity hypoventilation syndrome (OHS). In its most severe form, when both SAS and OHS are present, it is called the Pickwickian syndrome. In our series 59 morbidly obese patients with respiratory insufficiency secondary to obesity underwent gastric surgery for weight reduction. Fourteen had OHS, 19 had SAS and 26 had both. Of these, two patients died of postoperative complications and one died at five weeks with an inconclusive autopsy, totalling an operative mortality rate of 3.4 per cent and a total mortality of 5.1 per cent. In our overall experience morbidly obese patients lost 67 per cent of excess weight after gastric procedures. In conclusion, surgically induced weight loss will markedly improve or correct respiratory insufficiency secondary to obesity. It will improve arterial oxygenation, minimize CO2 retention, expand lung volumes, correct polycythemia, and reduce apnea frequency. The magnitude of changes in these variables is clinically significant. Therefore, respiratory insufficiency of obesity should be considered a major indication for an aggressive approach to weight reduction. The jejunoileal bypass and unbanded gastroplasty operations have an unacceptable incidence of complications or failure, respectively. There is a high degree of recidivism following dietary programs. Sweets eaters will not do well with a gastroplasty procedure. Gastric bypass for individuals addicted to sweets or the vertical banded gastroplasty for "gorgers" are currently our procedures of choice and are associated with the average loss of two thirds of excess weight and correction of breathing problems associated with morbid obesity.
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PMID:Pulmonary function in morbid obesity. 331 3

1. Sedatives such as the benzodiazepines and alcohol reduce upper airway muscle activity. We hypothesized that a sedating antihypertensive, alpha-methyldopa, might have similar effects. To investigate this hypothesis we studied the effect of alpha-methyldopa on alae nasi electromyographic (EMG) activity during hypercapnia. 2. We studied ten healthy subjects and three subjects with obstructive sleep apnoea during CO2-stimulated breathing. In a preliminary study four subjects demonstrated a fall in alae nasi EMG activity 4 h after the ingestion of 500 mg of alpha-methyldopa during CO2 rebreathing. 3. In six additional normal subjects and three subjects with obstructive sleep apnoea, we studied the alae nasi EMG activity during steady-state hypercapnia with PCO2 held constant 5 torr (0.7 kPa) above baseline. On 2 separate days we studied subjects before and 2 h after they had ingested 750 mg of alpha-methyldopa or placebo. 4. In the normal subjects the mean alae nasi EMG activity fell by 34% 2 h after ingestion of alpha-methyldopa (P less than 0.05) without a change in other ventilatory parameters. 5. In the sleep apnoea group the individual mean alae nasi EMG activity fell 16-49%, with ventilation and tidal volume falling in one patient. 6. We conclude that alpha-methyldopa selectively reduces upper airway motor activity.
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PMID:Alpha-methyldopa selectively reduces alae nasi activity. 337 Sep 22

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
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PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

Primary alveolar hypoventilation is a rare syndrome of unknown origin, characterized by a dysfunction of the automatic respiratory pattern in spite of normal lungs and in the absence of mechanical ventilatory defects. A reduction of the ventilatory response to CO2 is regularly found, and cardiac failure is common. The differential diagnosis mainly concerns the sleep apnoea syndrome. The usual treatments have little effectiveness.
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PMID:[Primary alveolar hypoventilation. Clinical aspects and diagnostic problems. Apropos of a case]. 367 71

Based on results on central chemosensitivity in cats, paired stimuli were applied for therapy to infants with central respiratory insufficiency of various degrees. An unspecific respiratory stimulus, e.g. light for 1 s, was followed by a jet of either O2 or 2% CO2 in O2 for 1.5 s. The unspecific and the chemical stimuli were interspaced by 0.5 s. The combined stimulation was repeated every 10 s. The program was triggered by using threshold values of transcutaneous pO2. In infants with intratrachial tubes or tracheostoma we used the end tidal pCO2 for triggering the stimulation. The method could prevent hypoxemia during sleep in non-ventilated subjects with sleep apnea syndromes or in infants with severe hypoxemia during sleep after being rescued from Sudden Infant Death Syndrome (SIDS). In patients with Ondine's Curse Syndrome (OCS) with its CO2 insensitivity, paired stimuli were used in order to condition the chemical function of the respiratory system. Polysomnograms from 310 clinically healthy infants including healthy siblings of SIDS victims revealed instability of arterial pO2 and low CO2 sensitivity during sleep within the second month and the fourth to ninth month of life, respectively. These data challenge the described method as a potential preventive or therapeutic measure to defeat SIDS and sleep apnea syndromes in conjunction with disturbed chemical regulation of respiration.
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PMID:Transcutaneous monitoring as trigger for therapy of hypoxemia during sleep. 367 92

We have emphasized the mechanisms and consequences of sleep state effects on the manifestation of a sensitive apneic threshold. In the absence of the stabilizing influences of wakefulness, even the healthy person is vulnerable to instabilities and ventilatory control as maintenance of a rhythmic breathing pattern becomes overwhelmingly dependent on CO2. This sleep-induced unmasking of the depressant effects of hypocapnia contrasts with the relatively minor effects of sleep on the ventilatory response to a wide variety of other acute or chronic ventilatory stimuli or inhibitors. This combination of an apneic threshold with a maintained hypoxic (and asphyxic) responsiveness during non-REM sleep probably explains much of the periodic breathing in hypoxic sleep in adults and in newborns. Furthermore, applying acute hypoxia to persons with upper airways that are susceptible to collapse, i.e., snorers, showed that fluctuating chemical stimuli and the accompanying instability in ventilatory control during sleep can cause obstructive apnea, at least under conditions where chemoreceptor stimuli are sufficient to initiate some inspiratory effort but insufficient to insure a completely patent upper airway. We emphasize that chemoreceptor-induced instability and/or apnea probably plays little or no role in the induction of many other varieties of sleep apnea including most obstructive sleep apneas and perhaps even in some types of nonobstructive apnea. The consequences of these chemoreceptor-induced instabilities are, of course, substantial in terms of impairment of pulmonary gas exchange and the precipitation of events that contribute significantly to the development of chronic cor pulmonale.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A sleep-induced apneic threshold and its consequences. 371 65


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