Parameters of resting and fMLP-induced LBCL were the co-primary variables in our study. The morning and evening chemiluminescence parameters like rCL, pCL and tCL as well as FRAP were higher in OSAS patients in comparison with controls. Nevertheless, we did not find any differences between morning and evening LBCL parameters between and within the groups of OSAS, CPAP-OSAS and the matched controls. Moreover, LBCL did not rise significantly after polysomnography controlled sleep in the subgroup of patients with severe untreated OSAS. Therefore, our results suggest that OSAS related IH did not enhance ROS production by blood PMNs and monocytes. This finding is in contrast with the results of two previous studies showing increased ROS production from isolated PMNs (following stimulation with fMLP) and some subpopulations of whole blood monocytes (resting and phorbol myristate acetate – activated) of OSAS patients [14, 15].
Apart from the absence of cell isolation procedures and the usage of monoclonal antibodies to surface cell markers possibly altering PMNs and monocytic responsiveness to agonist stimulation, there were other significant differences between the protocols of our study and the aforementioned. In previous studies, the control subjects were not matched to OSAS patients in respect to age, BMI, cigarette smoking habits in addition to comorbidity [14, 15]. Moreover, both investigations did not provide information concerning concomitant pharmacologic treatment [14, 15]; furthermore, experiments on the effect of OSAS related IH on monocytic activity were based on only 8 to 10 subjects out of the 18 enrolled  devoid of an unambiguous selective criterion.
In view of the fact that the majority of OSAS patients are obese often developing a variety of cardiovascular and metabolic diseases [1, 2], there exists a challenge in finding appropriate control subjects, chiefly in respects to comorbidity and concomitant pharmacological treatment. In our study, we overcome this impediment by measuring LBCL prior to and following polysomnographic controlled sleep, formulating comparisons within and between study groups. These approaches act to possibly eliminate biases related to patient medication, intensifying the quality of our results in showing no priming or activation of blood phagocytes in untreated OSAS patients.
The sympathetic over activity in OSAS patients resulting in the rise of plasma norepinephrine and epinephrine levels [25–27] may perhaps be responsible in the insignificant changes between evening and morning blood LBCL in OSAS patients. Reports have demonstrated a higher morning (following awakening) plasma norepinephrine concentration than those before sleep in OSAS patients by 24% . Nonetheless, a night of successful CPAP therapy resulted in a down-regulation of sympathetic activity as well as a decrease in circulating catecholamines by 20% . Catecholamines in vitro, especially epinephrine at physiologic levels revealed concentration dependent inhibition of fMLP-induced degranulation and superoxide radical production by human PMNs [28–30]; with a capability of suppressive monocytic activity as well [31, 32]. Therefore, exposition of circulating phagocytes to increased concentrations of catecholamines may result in their insusceptibility to the priming effect of IH in respiratory burst, assuming responsibility for the negative results in untreated OSAS patients. On the other hand, the observation of rapidly reversible sympathetic over-activation due to successful treatment  elucidates the indifferences among morning and evening LBCL in CPAP-OSAS group. This may result from the simultaneous reduction of IH episodes along with plasma catecholamine suppression, together with a rapid turnover of circulating PMNs; strongly supported by a recent study demonstrating the inhibitory effect of exercise on hypobaric hypoxia-induced enhancement of ROS production by PMNs in healthy volunteers . It cannot be excluded that our OSAS patients encountered an inadequate amount of apneas/hypopneas, consequently observing insufficient blood desaturations to prime PMNs to fMLP stimulation. In the abovementioned study, overnight hypobaric hypoxia decreased the average SaO2 from a baseline of 98% to 93% concluding a high altitude stay .
A decreased average SaO2 (84%) along with minimal SaO2 (68%) was evident in our investigated patients, particularly those with severe OSAS, due to numerous transient desaturations. The activity of two secondary variables (FRAP and H2O2 activity in the whole blood) in OSAS patients after sleep was compatible to the results of LBCL. We did not observe sleep-induced ROS overproduction in the blood (LBCL, H2O2 activity) of untreated OSAS patients, therefore no suppression of morning FRAP was noted. On the other hand, resistance of FRAP to 1 h in vitro incubation with high concentrations of H2O2 suggests strong antioxidant plasma capacity. Therefore, FRAP suppression related to significant expenditure of circulating antioxidants with high Fe3+ reducing activity will occur in vivo in the case of large and long (probably longer than one night) systemic ROS overproduction.
The results of our study suggest that circulating phagocytes (PMNs and monocytes) are not the main culprit of OSAS consequences in the human body. It does not exclude augmented ROS production and activation of the systemic ROS signaling [7, 14, 34]. Circulating phagocytes probably do not take part in oxidative stress, which does not synonymously reject the oxidative stress presence in OSAS patients. It can take place near or exactly in blood vessel endothelium, which can significantly accelerate atherosclerosis.