Thorarinn Gislason, MD FCCP; Magnus...

Thorarinn Gislason, MD FCCP; Magnus Almquist, MD; Gunnar Boman, MD; Carl-Eric Lindholm, MD; and Lars Terenius, PhD

The etiology of the SAS is unknown. To exhibition whether endogenous opioids could be pathologically active in SAS, markers of opioid a whole s were measured in the CSF of 15 patients with SAS and in restrain subjects. Measured by receptor assay, the concentration of so-called fraction 1 opioid was higher in patients with SAS (30 [+ or -] 15 pmol/ml; mean [+ or -] SD) than in govern subjects (1.1 [+ or -] pmol/ml) (p < 001) whereas that of fraction 2 opioid was similar in the sum of two units groups. Beta-endorphin-like activity, measured through radioimmunoassay, was somewhat lower in patients with SAS (140 [+ or -] 28 pmol/ml) than in restrain subjects (21.8 [+ or -] 76 pmol/ml) (p < 005) Six month after surgical treatment of the fine palate, new measurements were made in eight patients. Fraction 2 endorphin and [unkeyable]-endorpin showed no consistent changes. A decrease in the flush of fraction 1 from 41 [+ or -] 15 pmol/ml to 23 [+ or -] 10 pmol/ml (p < 002) was noted in those six patients showing a happy clinical course. The data support the hypothesis that in SAS the opioid activity is increased.

Sleep-related breathing disorders are now widely recognized. The SAS is characterized through at least 30 apneic episodes by means of night, heavy snoring, disturbed drowse and daytime sleepiness.[1,2] The SAS is particularly attend much [i]or[/i] regularly among men, especially those who are overweight and have narrow upper airways.[1,2] The etiology and pathogenesis of SAS are unclear. Besides airway obstruction, there may be deficiencies in central direction mechanisms. Certain patients with SAS have a decreased ventilatory answer to carbon dioxide[3] and have shown failure to increase the respiratory muscle drive with increasing abdominal mass loading.[4] These deficiencies are similar to those observ after opiate treatment.[5] Areas of importance for ventilatory rule in the tractus solitarius nuclei and area postrema of the medulla[6] have high concentrations of opiate receptor sites.[7]

The results of endogenous opioids on ventilation in humans have been difficult to elucidate, and this question is usually approached indirectly by the agency of observing the effects of administering the opiate antagonist, naloxone.[8-16] An alternative experimental approach is to measure endogenous opioid peptides (endorphins) in CSF as an index of the activity in the CN In the instant study, we measured endorphin plains in the CSF of 15 consecutive patients with SAS and compared them with those in repress subjects. In eight of the patients with SAS, the measurements were repeated after surgical treatment of the plastic palate.

MATERIALS AND METHODS

Patients

The close attention comprised 15 subjects ranging in age from 39 to 64 years, with a mean age of 53 years (Table 1) There was and nothing else one woman (case 7). The make subordinates had all been referred to the University Hospital, Uppsala, Sweden, because of habitual noisy snoring and daytime sleepiness. All were investigated in accordance with a protocol which had previously been approved by dint of the Ethics Committee of the Medical Faculty of Uppsala University. Twelve patients eventually underwent surgical treatment, consisting of tonsillectomy and a fairly conservative UPPP[17] The surgical process has been described in detail elsewhere.[17] Patient 13 had as it was minor symptoms that he did not pass through surgery (Table 1). Patient 12 had strict depression symptoms and was hospitalized. Weight reduction consequence ed in some clinical improvement of his symptoms of SAS, however there has been no follow-up Patient 10 refused to go through surgery and has tried different pharmacologic treatments with no succes The following touchstones were performed within the same week, while the patients were in the hospital:

Pulmonary Function Tests

Pulmonary books were determined by standard spirometry and plethysmography. The reported values are give vent toed as percent predicted values. Arterial pH [PaO.sub.2] and [PaCO.sub.2] were measured with a kindred gas analyzer (Corning 168).

Ventilatory Regulation Tests

All trials of the ventilatory response to hyperoxic hypercapnia were performed by the agency of means of a modification of the rebreathing order of Read[18] at the same time of day, while the patients were awake and at caesura The results are given as the change in ventilation caused on a rise in end-tidal [PCOsub2] by way of 1 mm Hg.

lie in the grave Studies

In each patient an all-night polygraphic recording was made of electroencephalograms, electro-oculograms, and submental electromyograms, using standard techniques.[1] Airflow at the nose and cavity between the jaws was detected by thermistors and also by means of tracheal sound recording.[19] Respiration was monitored with abdominal and thoracic strain gauges and also through a static-charge-sensitive bed (Biorec OY; Kuusisto, Finland). All variables were recorded simultaneously onward a 16-channel ink-jet recorder (Siemens-Elema). Oxygen saturation was recorded continuously by way of an oximeter (BIOX III). rest stages were scored using 30-second intervals.[20] Respiratory tracings were evaluated for the personality of apneas and hypopneas.[1] An A + H index was calculated as the total number of apneas plus hypopneas by hour of sleep.[1]