Mohammed A Alzoghaibi1, Ahmed S Bahammam. 1. Department of Physiology, The University Sleep Disorders Center, College of Medicine and the Center of Excellence in Biotechnology Research, King Saud University, Riyadh, Saudi Arabia.
Abstract
PURPOSE: The purpose of this study was to examine the effects of one night of continuous positive airway pressure (CPAP) therapy on oxidative stress (lipid peroxidation) levels and the antioxidant activities of superoxide dismutase (SOD) in hypertensive patients with severe obstructive sleep apnea (OSA). METHODS: The study group consisted of 34 hypertensive, non-smoking patients with a mean age of 45.09 ± 11.77 years, body mass index of 37.4 ± 8.4 kg/m(2), apnea hypopnea index of 79.17 ± 31.35/h, and desaturation index of 55.07 ± 27.06/h. Patients included in the study were not on medications that may affect antioxidant activity. Patients spent four nights in the sleep disorder center as follows: night 1, an adaptation night; night 2, a diagnostic night; night 3, CPAP titration night; and night 4, a therapeutic night for CPAP treatment. Blood samples were collected in the morning upon awakening on nights 2 and 4 and were immediately transferred to the laboratory for SOD and lipid peroxidation measurements. Oxidative stress levels were quantified by measuring thiobarbituric acid reactive substances. SOD enzymatic activity was measured using a purely chemical system based on NAD(P)H oxidation. RESULTS: Mean SOD concentrations were not significantly different in pre-and post-CPAP treatment (0.22 ± 0.09 vs. 0.22 ± 0. U/ml, respectively). However, CPAP treatment significantly inhibited lipid peroxidation levels (2.81 ± 0.27 vs. 2.47 ± 0.35 mmol/ml, respectively, p < 0.005). CONCLUSION: The present study supports the theory that CPAP therapy decreases the levels of oxidative stress in OSA patients but may not affect antioxidant defense.
PURPOSE: The purpose of this study was to examine the effects of one night of continuous positive airway pressure (CPAP) therapy on oxidative stress (lipid peroxidation) levels and the antioxidant activities of superoxide dismutase (SOD) in hypertensivepatients with severe obstructive sleep apnea (OSA). METHODS: The study group consisted of 34 hypertensive, non-smoking patients with a mean age of 45.09 ± 11.77 years, body mass index of 37.4 ± 8.4 kg/m(2), apnea hypopnea index of 79.17 ± 31.35/h, and desaturation index of 55.07 ± 27.06/h. Patients included in the study were not on medications that may affect antioxidant activity. Patients spent four nights in the sleep disorder center as follows: night 1, an adaptation night; night 2, a diagnostic night; night 3, CPAP titration night; and night 4, a therapeutic night for CPAP treatment. Blood samples were collected in the morning upon awakening on nights 2 and 4 and were immediately transferred to the laboratory for SOD and lipid peroxidation measurements. Oxidative stress levels were quantified by measuring thiobarbituric acid reactive substances. SOD enzymatic activity was measured using a purely chemical system based on NAD(P)H oxidation. RESULTS: Mean SOD concentrations were not significantly different in pre-and post-CPAP treatment (0.22 ± 0.09 vs. 0.22 ± 0. U/ml, respectively). However, CPAP treatment significantly inhibited lipid peroxidation levels (2.81 ± 0.27 vs. 2.47 ± 0.35 mmol/ml, respectively, p < 0.005). CONCLUSION: The present study supports the theory that CPAP therapy decreases the levels of oxidative stress in OSA patients but may not affect antioxidant defense.
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