| Background:Sleep apnea syndrome (SAS) is a common sleep disorder, prevalent in approximately 2% to 4% of adult people. Its frequency increases with increased age and body mass index (BMI), and the incidence rate for men is about two to nine times than in women. The patients with SAS suffer from fragmented sleep and decreased arterial oxygen saturations, but it is still unclear whether SAS is a cause of mental changes and psychiatric abnormalities in some of these patients. Previous reports have linked SAS with cardiovascular morbidity, depression, anxiety and cognitive deficits. The severity and mechanisms of these impairments are yet uncertain. Previous studies demonstrated several lines of pharmacological, neurobehavioral and therapeutic evidence implicated nitric oxide (NO), serotonin (5-HT) and catecholamines (CA) in the pathogenesis of regulation of sleep and respiration. Moreover, SAS has been shown to aggregate significantly within families. Although there have been many researches had paid attention to the genotypic markers for this condition, no certain genetic vulnerabilities for SAS have been found. The serotonin transporter (5-HTT) reuptakes serotonin into the pre-synaptic neuron. Most antidepressants block the action of 5-HTT and can also treat the major depression or sleep disorders. Two common polymorphisms have been described in the 5-HTT gene: a deletion/ insertion of 44bp in the promoter region approximately 1kb upstream of the transcription site (5-HTTLPR) and a Variable-Number-Tandem-Repeat (VNTR) region containing 9, 10 or 12 copies of a 17bp repeat element located in intron 2 (5-HTTVNTR). Therefore, we evaluated the roles of the 5-HTTLPR and VNTR in SAS and impaired sleep or daytimefunctions of this condition. Study objectives:To evaluate the association between SAS and sleep disturbant patterns, psychological abnormalities or cognitive impairment. Another purpose of this study was to evaluate the possible roles of nitric oxide, serotonin and catecholamines in the pathogenesis of sleep apnea. The third objective was to identify polymorphisms of the serotonin transporter gene and to find out whether there was correlation between any such polymorphisms and the occurrence of sleep apnea. Methods:The study comprised 78 patients diagnosed as SAS who refered to the sleep laboratories and then underwent a whole-night polysomno-graphic examination. The study population was stratified into subgroups based on MinSaO2 and BMI. Of 78 patients with SAS, 45 subjects completed psychological and cognitive examination. Thirty healthy controls underwent the same examination. In 45 patients and 30 healthy controls, NO, 5-HT and CA levels were measured in peripheral venous blood samples by chemiluminescence and high-performance liquid chro-matography (HPLC), respectively. The frequencies of the different forms of the genotypes and alleles of 5-HTT gene was analysed in 45 patients with SAS and 55 healthy controls. Results:1. Compared with healthy controls, SAS patients suffered more from disturbed or fragmented sleep, (i). In addition to intermittent nocturnal hypoxemia and apneic attacks, stages of sleep were also disturbed, such as decreased SWS% and REM%, increased S1% or S2% and brief arousal frequency from sleep, etc. And the latency of sleep in SAS group was significantly shorter than that in control group (P<0.05).(ii). The sleep disturbance within the group of severe nocturnal hypoxemia (Min SaO2<60%) was significantly more prominent than in both mild and moderate hypoxemic groups (P<0.05). (iii). The sleep structure, respiration and heart rate were most disturbed in the group of severe fat patients (BMI>30.01kg/m2) than in the two other groups in SAS patients (P<0.05).2. Compared with, healthy controls, SAS patients suffered from striking clinical features, including impaired daytime functions, (i). The common clinical complaints were snoring, unrefreshing sleep, daytime sleepiness, choking episodes, etc. (ii). The total scores of ESS in SAS group were significantly hig...
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