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)

We investigated the mechanisms of the beneficial effect derived from progesterone therapy for sleep apnea syndrome (SAS). Nine patients with SAS were treated for 7 days with chlormadinone acetate (CMA), a respiratory stimulant known to increase not only CO2 and hypoxic chemosensitivity but also respiratory drive response for ventilatory loading. They were examined as to sleep events and ventilatory control during wakefulness before and during CMA treatment. Apnea-hypopnea index was significantly reduced from 51.1 +/- 5.7 to 43.6 +/- 8.1 episodes/h (p less than 0.05). The ratio of desaturation time with more than 4% SaO2 fall to total sleep time was diminished in seven of nine patients, and its mean value decreased from 44.9 +/- 8.6 to 28.7 +/- 8.1% (p less than 0.05). Both hypercapnic ventilatory response (HCVR) and load response during wakefulness were significantly increased, although isocapnic hypoxic ventilatory response (HVR) was not significantly enhanced by CMA. The degree of augmentation in awake load response as well as in HCVR was positively correlated with that of improvement in sleep-disordered breathing. Moreover, patients who did not show amelioration in oxygen desaturation were found to be incapable of increasing load response despite increased HCVR. We conclude that CMA therapy for sleep apnea syndrome is effective in the patients whose load response as well as respiratory control activity are augmented during wakefulness.
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PMID:Progesterone therapy for sleep apnea syndrome evaluated by occlusion pressure responses to exogenous loading. 246 68

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

The effects of oxygen administration were studied in 10 patients with severe obstructive lung disease. Sleep variable and gas exchanges were measured during two nights: one when they were breathing environmental air, the other when they were receiving oxygen. Carbon dioxide saturation and partial pressure measured by the transcutaneous method were continuously recorded. Sleep was perturbed in all patients, but despite wide interindividual variations its amount and quality were improved by oxygen. None of the patients had sleep apnoea syndrome. Oxygen administration was accompanied by a nocturnal increase in carbon dioxide pressure that was about twice as high as that observed under environmental air. Thus, in patients with chronic obstructive lung disease without concomitant infection suppression of the hypoxic stimulus by oxygen therapy seems to result in an increase in carbon dioxide partial pressure identical with the increase produced by sleep alone. Correlations between diurnal and nocturnal oxygen saturation and carbon dioxide partial pressure indicate that patients with the highest degree of hypoxia and hypercapnia in daytime have the most severe nocturnal blood gas disorders.
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PMID:[Chronic obstructive bronchopneumopathies. Changes in carbon dioxide pressure during sleep in environmental air and with oxygen]. 252 37

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

To assess the relative contributions of age, gender, obesity, pulmonary function, and the severity of sleep-induced respiratory abnormalities to the development of alveolar hypoventilation in patients with occlusive sleep apnea syndrome, prospective data from III patients with occlusive sleep apnea were analyzed by stepwise logistic and multiple regression techniques. The significant variables in a logistic regression model predicting the presence of hypercapnia were daytime arterial oxygen pressure (PaO2; p less than 0.0001) and gender (p less than 0.04), the latter reflecting the higher number of hypercapnic women in our patient population. Multiple regression analysis performed in the hypercapnic group to study the determinants of the severity of elevation of arterial carbon dioxide tension (PaCO2) revealed significant contribution from the PaO2, the apnea-plus-hypopnea index (AHI), and the percent predicted forced vital capacity (r2 = 0.56; p less than 0.0001), whereas in the normocapnic patients, PaCO2 related to PaO2 only. These results suggest that daytime hypoxemia, mechanical impairment of the respiratory system due to obesity or obstructive airway disease (or both), and the severity of sleep-induced respiratory abnormalities as assessed by AHI contribute to the severity of carbon dioxide retention in patients with occlusive sleep apnea in a multifactorial fashion.
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PMID:Determinants of hypercapnia in occlusive sleep apnea syndrome. 311 99

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


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