Abstract
BackgroundObstructive sleep apnea syndrome (OSAS) is a recognized risk factor for cardiovascular morbidity and mortality, perhaps due to causative exacerbations of systemic oxidative stress. Putative oxidative stress related to numerous episodes of intermittent hypoxia, may be an oxidants chief driving force in OSAS patients.MethodsWe assessed the resting and n-formyl-methionyl-leucyl-phenylalanine (fMLP)- induced whole blood chemiluminescence (as a measure of oxidant production by polymorphonuclear leukocytes and monocytes), ferric reducing ability of plasma (FRAP) and H2O2 generation in the whole blood of 27 untreated OSAS patients, 22 subjects after a night of CPAP therapy and 11 controls without OSAS. All of them were matched to age, BMI (body mass index) and smoking habits. All parameters were measured before and after polysomnography-controlled sleep, individual results were obtained as a mean from duplicated experiments.ResultsNo significant differences were distinguished between evening and morning blood chemiluminescence, H2O2 activity and FRAP within and between all three study groups.For instance patients with untreated OSAS had similar morning and evening resting whole blood chemiluminescence (2.3 +/- 2.2 vs. 2.4 +/- 2.2 [aU·10-4 phagocytes]), total light emission after stimulation with fMLP (1790 +/- 1371 vs. 1939 +/- 1532 [aU·s·10-4 phagocytes]), as well as FRAP after 3 min. plasma incubation (602 +/- 202 vs. 671 +/- 221 [uM]). Although, in the subgroup of 11 patients with severe OSAS (apnea/hypopnea index 58 +/- 18/h and oxygen desaturation index 55 +/- 19/h), the morning vs. evening resting chemiluminescence and total light emission after stimulation with fMLP observed a propensity to elevate 2.5 +/- 2.7 vs. 1.9 +/- 1.8 [aU·10-4 phagocytes] and 1778 +/- 1442 vs. 1503 +/- 1391 [aU·s·10-4 phagocytes], respectively, these did not attain statistical significance (p > 0.05).ConclusionOur investigation exposed no evidence in the overproduction of oxidants via circulating phagocytes, once considered a culprit in the oxidative stress of OSAS patients.
Highlights
Obstructive sleep apnea syndrome (OSAS) is a recognized risk factor for cardiovascular morbidity and mortality, perhaps due to causative exacerbations of systemic oxidative stress
We found that the apnea/hypopnea episodes during sleep did not change the morning and evening intensity of the resting as well as fMLP-induced luminol enhanced whole blood chemiluminescence (LBCL), ferric reducing ability of plasma (FRAP) and blood H2O2 activities in the OSAS patients
The results of our study suggest that circulating phagocytes (PMNs and monocytes) are not the main culprit of OSAS consequences in the human body
Summary
Obstructive sleep apnea syndrome (OSAS) is a recognized risk factor for cardiovascular morbidity and mortality, perhaps due to causative exacerbations of systemic oxidative stress. Putative oxidative stress related to numerous episodes of intermittent hypoxia, may be an oxidants chief driving force in OSAS patients. The presence of obstructive sleep apnea syndrome (OSAS) is strongly associated with augmented morbidity and mortality from cardiovascular diseases including arterial hypertension, cardiac arrhythmias and ischemic heart disease [1,2]. There appears to be practicable links between OSAS and occurrences such as apnea-induced intermittent hypoxia (IH) of tissues, sympathetic over activities during sleep [5,6] as well as putative oxidative stress in relation to the systemic inflammatory response [6,7]. The in vitro incubation of whole blood under decreased partial oxygen pressure (pO2 ≤ 46 mm Hg) resulted in the degranulation of PMNs [8] and increased ROS production [9].
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