Search

Obstructive sleep apnoea (OSA) is associated with a variety of nightly stresses, including intermittent hypoxaemia, oxidative stress and sleep fragmentation. Heat-shock proteins (HSPs) are upregulated in response to an array of environmental and metabolic stresses. We hypothesized that the OSA-related stresses would affect the expression of HSP70 in monocytes. Basal (30 min, at 37 degrees C), heat stress-induced HSP70 (30 min, at 43 degrees C) and basal tumour necrosis factor-alpha (TNF-alpha) were determined by flow cytometry in monocytes of 10 patients with OSA and 10 controls matched by age, gender and body mass index. Oxidative stress was determined by thiobarbituric acid-reactive substances (TBARS) and antioxidant paraoxonase-1 activity. Basal HSP70 expression was 1.8-fold higher in patients with OSA as compared with controls (P < 0.0005) and was significantly positively correlated with TBARS (r = 0.56, P < 0.009). However, induction of HSP70 in response to heat stress treatment was lower by 40% in OSA monocytes as compared with controls (P < 0.0003). Furthermore, heat stress-induced HSP70 expression was significantly negatively correlated with basal HSP70 expression independently of apnoea severity (r = -0.69, P < 0.0006). Also, basal intracellular TNF-alpha expression was inversely correlated with heat-shock-induced HSP70 (r = -0.78, P < 0.015) in OSA monocytes but not in controls. In conclusion, basal HSP70 overexpression that is a protective mechanism indicative of disease-associated stress was significantly higher in patients with OSA and was correlated with oxidative stress. On the other hand, in response to a defined heat-stress treatment, the induction of HSP70 was lower in patients with OSA, indicative of a possible maladaptive response to an acute stress. Correlations with oxidative stress and TNF-alpha further support this conclusion.

Background: Sleep apnea syndrome is an important risk factor for atherosclerosis and cardiovascular morbidity and so is cigarette smoking. In both atherosclerosis and cardiovascular disease, oxidative stress and inflammation have been implicated as underlying pathophysiologic mechanisms. We investigated oxidative stress and inflammatory markers in 70 non-smoking and smoking patients with sleep apnea., Methods: Thirty-five sleep apnea patients aged 20-60 years who smoke 20 or more cigarettes/day and for at least 5 years were individually matched by gender, age (+/-5 years), body mass index (BMI; categorized as, 'normal weight', 'overweight', and 'obese'), sleep apnea severity (categorized as 'mild', 'moderate', and 'severe'), and presence of cardiovascular diseases, with 35 patients who never smoked. Blood samples were drawn after an overnight fasting for determination of lipids profile, oxidative stress markers thiobarbituric acid reactive substances, peroxides and paraoxonase-1 and inflammatory markers C-reactive protein, ceruloplasmin, and haptoglobin., Results: Smokers showed significantly higher levels of C-reactive protein, ceruloplasmin, and haptoglobin and triglycerides and lower levels of high-density lipoprotein (HDL) cholesterol than non-smokers. There was a significant interaction effect between smoking and apnea severity on ceruloplasmin and HDL levels. Smokers with severe sleep apnea had the highest level of ceruloplasmin and the lowest level of HDL., Conclusion: There is a synergistic effect between cigarette smoking and sleep apnea on some of the biochemical cardiovascular risk markers. Patients with severe sleep apnea who smoke are at a greater cardiovascular risk than smokers with mild-moderate sleep apnea and patients who do not smoke.

Obstructive sleep apnoea (OSA) is associated with a variety of nightly stresses, including intermittent hypoxaemia, oxidative stress and sleep fragmentation. Heat-shock proteins (HSPs) are upregulated in response to an array of environmental and metabolic stresses. We hypothesized that the OSA-related stresses would affect the expression of HSP70 in monocytes. Basal (30 min, at 37 °C), heat stress-induced HSP70 (30 min, at 43 °C) and basal tumour necrosis factor-α (TNF-α) were determined by flow cytometry in monocytes of 10 patients with OSA and 10 controls matched by age, gender and body mass index. Oxidative stress was determined by thiobarbituric acid-reactive substances (TBARS) and antioxidant paraoxonase-1 activity. Basal HSP70 expression was 1.8-fold higher in patients with OSA as compared with controls ( P < 0.0005) and was significantly positively correlated with TBARS ( r = 0.56, P < 0.009). However, induction of HSP70 in response to heat stress treatment was lower by 40% in OSA monocytes as compared with controls ( P < 0.0003). Furthermore, heat stress-induced HSP70 expression was significantly negatively correlated with basal HSP70 expression independently of apnoea severity ( r = −0.69, P < 0.0006). Also, basal intracellular TNF-α expression was inversely correlated with heat-shock-induced HSP70 ( r = −0.78, P < 0.015) in OSA monocytes but not in controls. In conclusion, basal HSP70 overexpression that is a protective mechanism indicative of disease-associated stress was significantly higher in patients with OSA and was correlated with oxidative stress. On the other hand, in response to a defined heat-stress treatment, the induction of HSP70 was lower in patients with OSA, indicative of a possible maladaptive response to an acute stress. Correlations with oxidative stress and TNF-α further support this conclusion. [ABSTRACT FROM AUTHOR]

The article presents a study to assess the effect of long-term modified Herbst mandibular advancement splint (MAS) treatment on obstructive sleep apnea (OSA), oxidative stress markers, and on endothelial function (EF) in the U.S. The study was conducted to 16 subjects, consisting of 11 men and 5 women, wherein 12 of whom were said to have completed an evaluation for a year. Results show that the Herbst MAS's efficacy justified the performance of larger randomized controlled trials.

The article discusses an association between cardiovascular diseases and obstructive sleep apnea (OSA). It shows the effect of reactive oxygen species (ROS) and oxidative stress on patients with OSA. It assesses the inducement of cardiovascular consequences of OSA by sympathoexcitation and oxidative stress/inflammation. Other risk factors of OSA are identified, including hypertension, insulin resistance and diabetes mellitus.

The authors respond to a commentary by M. Kohler and J. R. Stradling on the cardiovascular consequences of obstructive sleep apnea (OSA). They criticize the commentary for ignoring a literature linking sympathetic activation (SA) with oxidative stress. They also stress the evidence that reactive oxygen species (ROS) initiate SA and regulate sympathetic outflow from autonomic ganglia.