阻塞性睡眠呼吸暂停低通气综合征患者抗氧化能力的研究
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摘要
目的:研究OSAHS患者的血清抗氧化能力及nCPAP治疗对OSAHS患者血清抗氧化能力的影响。
方法:95例入选者经PSG监测,按睡眠呼吸紊乱严重程度进行分组:正常对照组(26例)、单纯性鼾症组(16例)、轻度OSAHS组(11例)、中度OSAHS组(21例)、重度OSAHS组(21例)。在PSG监测当晚及次晨抽取外周静脉血用比色法测定血清抗氧化物超氧化物歧化酶(SOD)、维生素E (VitE)、谷胱甘肽过氧化物酶(GSH-PX)、总抗氧化能力(T-AOC)。对比正常对照组、单纯性鼾症组、OSAHS组三组间抗氧化物水平的差异,分析各抗氧化物水平与AHI之间的相关性。开展nCPAP干预实验,对接受/未接受nCPAP治疗的中重度OSAHS患者随访3个月,复查PSG及血清学指标。
结果:(1)正常对照组与单纯性鼾症组2组间血清SOD、VitE、GSH-PX、T-AOC差异均无统计学意义(p均>0.05)。OSAHS组血清SOD、VitE、T-AOC水平均比正常对照组及单纯性鼾症组低(p均<0.01)。3组间血清GSH-PX水平差异无统计学意义(F=2.99,p>0.05)。(2)OSAHS组晨起血清T-AOC较睡前低(p<0.01),正常对照组及单纯性鼾症组晨起血清T-AOC与睡前时比较,差异无统计学意义(p>0.05)。(3)相关分析:SOD、VitE、GSH-PX、T-AOC与AHI均呈负相关关系(r = -0.517 p<0.01;r = -0.717 p<0.01;r = -0.623 p<0.01;r = -0.765 p<0.01)。(4)中重度OSAHS患者中,接受nCPAP治疗者随访3个月后,血清SOD、T-AOC升高(p均<0.01),VitE无变化(p>0.05)。未接受nCPAP治疗者随访3个月后,血清SOD、T-AOC、VitE无变化(p均>0.05)。
结论:OSAHS患者血清抗氧化能力减弱,且晨起时血清总抗氧化能力较睡前降低。OSAHS病情越严重,AHI值越大,血清抗氧化能力越弱。nCPAP治疗使OSAHS患者血清抗氧化物水平升高,可改善OSAHS患者血清抗氧化能力。
Objective to explore the antioxidant capacity in patients with obstructive sleep apnea-hypopnea syndrome(OSAHS) and impact of continuous positive airway pressure(CPAP) treatment. Method Following polysomnographic examination, 95 sbjucts were assigned to 5 groups: simple snores(16 case), mild OSAHS(11 case), moderate OSAHS(21 case), severe OSAHS(21 case), and control group(26 case). The serum level of superoxide dismutase(SOD)、vitamin E(VitE)、glutathione peroxidase(GSH-PX)、total antioxidant capability(T-AOC) were measured before and after sleep at the polysomnographic examination night. Of 42 patients with moderate or severe OSAHS, 22 patients who underwent nCPAP therapy were set as“nCPAP group”, 20 patients who did not undergo nCPAP therapy were set as“control group”. 7 patients were excluded from further follow-up. The assessment protocol was then repeated after 3 month,s follow-up. Results (1) There were no statistically significant differences of the serum level of SOD、VitE、GSH-PX、T-AOC between simple snores and control group. The serum level of SOD、VitE、T-AOC were significantly lower in OSAHS patient. The serum level of GSH-PX among 3 groups have no statistically significant differences(F=2.99,p>0.05). (2) The serum level of T-AOC was not different before and after sleep in simple snores and control group. OSAHS patient had less T-AOC after sleep. (3) Liner regression analysis showed the serum level of SOD, VitE ,GSH-PX,T-AOC were negatively correlated with AH(Ir = -0.517 p<0.01;r = -0.717 p<0.01;r = -0.623 p<0.01;r = -0.765 p<0.01). (4) After 3 months nCPAP therapy in OSAHS patients, the serum level of SOD、T-AOC were significantly increased. While there were no similar changes in OSAHS patients without nCPAP therapy. Conclusion OSAHS patients have less antioxidant capacity. Antioxidant capacity was negatively correlated with AHI. Antioxidant capacity could be improved by nCPAP therapy in OSAHS patients.
方法:95例入选者经PSG监测,按睡眠呼吸紊乱严重程度进行分组:正常对照组(26例)、单纯性鼾症组(16例)、轻度OSAHS组(11例)、中度OSAHS组(21例)、重度OSAHS组(21例)。在PSG监测当晚及次晨抽取外周静脉血用比色法测定血清抗氧化物超氧化物歧化酶(SOD)、维生素E (VitE)、谷胱甘肽过氧化物酶(GSH-PX)、总抗氧化能力(T-AOC)。对比正常对照组、单纯性鼾症组、OSAHS组三组间抗氧化物水平的差异,分析各抗氧化物水平与AHI之间的相关性。开展nCPAP干预实验,对接受/未接受nCPAP治疗的中重度OSAHS患者随访3个月,复查PSG及血清学指标。
结果:(1)正常对照组与单纯性鼾症组2组间血清SOD、VitE、GSH-PX、T-AOC差异均无统计学意义(p均>0.05)。OSAHS组血清SOD、VitE、T-AOC水平均比正常对照组及单纯性鼾症组低(p均<0.01)。3组间血清GSH-PX水平差异无统计学意义(F=2.99,p>0.05)。(2)OSAHS组晨起血清T-AOC较睡前低(p<0.01),正常对照组及单纯性鼾症组晨起血清T-AOC与睡前时比较,差异无统计学意义(p>0.05)。(3)相关分析:SOD、VitE、GSH-PX、T-AOC与AHI均呈负相关关系(r = -0.517 p<0.01;r = -0.717 p<0.01;r = -0.623 p<0.01;r = -0.765 p<0.01)。(4)中重度OSAHS患者中,接受nCPAP治疗者随访3个月后,血清SOD、T-AOC升高(p均<0.01),VitE无变化(p>0.05)。未接受nCPAP治疗者随访3个月后,血清SOD、T-AOC、VitE无变化(p均>0.05)。
结论:OSAHS患者血清抗氧化能力减弱,且晨起时血清总抗氧化能力较睡前降低。OSAHS病情越严重,AHI值越大,血清抗氧化能力越弱。nCPAP治疗使OSAHS患者血清抗氧化物水平升高,可改善OSAHS患者血清抗氧化能力。
Objective to explore the antioxidant capacity in patients with obstructive sleep apnea-hypopnea syndrome(OSAHS) and impact of continuous positive airway pressure(CPAP) treatment. Method Following polysomnographic examination, 95 sbjucts were assigned to 5 groups: simple snores(16 case), mild OSAHS(11 case), moderate OSAHS(21 case), severe OSAHS(21 case), and control group(26 case). The serum level of superoxide dismutase(SOD)、vitamin E(VitE)、glutathione peroxidase(GSH-PX)、total antioxidant capability(T-AOC) were measured before and after sleep at the polysomnographic examination night. Of 42 patients with moderate or severe OSAHS, 22 patients who underwent nCPAP therapy were set as“nCPAP group”, 20 patients who did not undergo nCPAP therapy were set as“control group”. 7 patients were excluded from further follow-up. The assessment protocol was then repeated after 3 month,s follow-up. Results (1) There were no statistically significant differences of the serum level of SOD、VitE、GSH-PX、T-AOC between simple snores and control group. The serum level of SOD、VitE、T-AOC were significantly lower in OSAHS patient. The serum level of GSH-PX among 3 groups have no statistically significant differences(F=2.99,p>0.05). (2) The serum level of T-AOC was not different before and after sleep in simple snores and control group. OSAHS patient had less T-AOC after sleep. (3) Liner regression analysis showed the serum level of SOD, VitE ,GSH-PX,T-AOC were negatively correlated with AH(Ir = -0.517 p<0.01;r = -0.717 p<0.01;r = -0.623 p<0.01;r = -0.765 p<0.01). (4) After 3 months nCPAP therapy in OSAHS patients, the serum level of SOD、T-AOC were significantly increased. While there were no similar changes in OSAHS patients without nCPAP therapy. Conclusion OSAHS patients have less antioxidant capacity. Antioxidant capacity was negatively correlated with AHI. Antioxidant capacity could be improved by nCPAP therapy in OSAHS patients.
引文
1. Svatikova A, Wolk R, Lerman L O, et al. Oxidative stress in obstructive sleep apnoea. Eur J Heart. 2005, 26:2435-2439.
2. Alzoghaibi M A, Bahammam A S. Lipid peroxides,superoxide dismutase and circulating IL-8 and GCP-2 in patients with sivere obstructive sleep apnea: a pilot study. Sleep Breath. 2005, 9: 119-126.
3. Ozturk L, Mansour B, Yuksel M, et al. Lipid peroxidation and osmotic fragility of blood cells in sleep apnea patients, Clin Chim Acta.2003,332(1-2):83-88
4. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med. 2000, 162:566-570.
5. Macmillan Crow LA, Crow JP, Thompson JA. Peroxynitrite-mediated inactireation of manganese superoxide dismutase involves nitration and oxidation of critical tyrosine residues. Biochemistry. 1998, 37:1613-1622.
6. Christou K, Markoulis N,Moulas AN, et a1. Reactive oxygen metabolites(ROMs) as an index of oxidative stress in obstructive sleep apnoea patients. Sleep Breath.2003, 7(3):105-110.
7. Lavie L, Vishnevsky A , Lavie P. Evidence for lipid peroxidation in obstructive sleep apnea. Sleep. 2004, 27(1):123—128.
8. Barcelo A, Miralles C, Barbe F, et al.Abnormal lipid peroxidation in patients with sleep apnea. Eur Respir J.2000, 16: 644–647.
9. Yamauchi M, Nakano H, Maekawa J, et al. Oxidative stress in obstructive sleep apnea. Chest, 2005,127:1647-1679.
10. Nanduri R, Prabhakar PHD. Sleep apnea: an oxidative stress?. Am J Respir Crit Care Med, 2002, 165(7):859—860.
11. Carpagnano GE, Kharitonov SA, Resta O, et al. Increased 8-isoprostane and ynterleukin-6 in breath condensate of obstructive sleep apnea patients. Chest, 2002, 122(4): 1162-1167.
12. 张红,乔华,王广发.阻塞性睡眠呼吸暂停低通气综合征患者呼出凝集气过氧化氢浓度.中华结核和呼吸杂志.2006,29(8):541-544.
13. A.Barcelo, F.Barbe, M.de la pena, et al. Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment. Eur Respir J.2006, 27:756-760.
14. Kostas Christou, Anargyros N Moulas, Chaido Pastaka, et al. Antioxdant capacity in obstructive sleep apnoea patients. Sleep Med. 2003,4:225-228.
15. 汤树海,潘晓军. 阻塞性睡眠呼吸暂停综合征患者体内氧自由基代谢的作用.山东大学学报(医学版).2006, 44(5)
16. 温燕,李家树,宋满景. 阻塞性睡眠呼吸暂停低通气综合征患者体内氧化应激状态的分析.中国实用医药.2007, 2(22): 20-22.
17. Gopalakrishnan A, Ji L L, Cirelli C. Sleep deprivation and cellular response to oxidative stress. Sleep. 2004, 27: 27-35.
18. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med. 2002, 165:934-939.
19. Robinson GR, Stradling JR, Davies RJ. Sleep 6: obstructive sleep apnoea/hypopnoea syndrome and hypertention. Thorax. 2004,59(12):1089-1094.
20. Chobanian AV, Bakris GI, Black HR, et al. the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003,289(19):2560-2572.
21. Griendling KK, FitzGerald GA.Oxidative stress and cardiorascular injury : Part I: Basic mechanisms and in vivo mornitoring of ROS. Circulation. 2003,108(17):1912-1916.
22. Peker Y, Hedner J, Norum J, et al. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow up. Am J Respir Crit Care Med. 2002,166(2):159-165.
23. Mooe T, Franklin KA, Holmstrom K, et al. Sleep-disordered breathing and coronary artery disease: long-term prognosis. Am J Respir Crit Care Med. 2001,164(10): 1910-1913.
1. Christou K, Markoulis N,Moulas AN, et a1. Reactive oxygen metabolites(ROMs) as an index of oxidative stress in obstructive sleep apnoea patients. Sleep Breath.2003, 7(3):105-110.
2. Lavie L, Vishnevsky A , Lavie P. Evidence for lipid peroxidation in obstructive sleep apnea. Sleep. 2004, 27(1):123—128.
3. Barcelo A, Miralles C, Barbe F, et al.Abnormal lipid peroxidation in patients with sleep apnea. Eur Respir J.2000, 16: 644–647.
4. Yamauchi M, Nakano H, Maekawa J, et al. Oxidative stress in obstructive sleep apnea. Chest, 2005,127:1647-1679.
5. Nanduri R, Prabhakar PHD. Sleep apnea: an oxidative stress?. Am J Respir Crit Care Med, 2002, 165(7):859—860.
6. Carpagnano GE, Kharitonov SA, Resta O, et al. Increased 8-isoprostane and ynterleukin-6 in breath condensate of obstructive sleep apnea patients. Chest, 2002, 122(4): 1162-1167.
7. 张红,乔华,王广发.阻塞性睡眠呼吸暂停低通气综合征患者呼出凝集气过氧化氢浓度.中华结核和呼吸杂志.2006,29(8):541-544.
8. A.Barcelo, F.Barbe, M.de la pena, et al. Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment. Eur Respir J.2006, 27:756-760.
9. Kostas Christou, Anargyros N Moulas, Chaido Pastaka, et al. Antioxdant capacity in obstructive sleep apnoea patients. Sleep Med. 2003,4:225-228.
10. Svatikova A, Wolk R, Lerman L O, et al. Oxidative stress in obstructive sleep apnoea. Eur J Heart. 2005, 26:2435-2439.
11. Alzoghaibi M A, Bahammam A S. Lipid peroxides,superoxide dismutase and circulating IL-8 and GCP-2 in patients with sivere obstructive sleep apnea: a pilotstudy. Sleep Breath. 2005, 9: 119-126.
12. Ozturk L, Mansour B, Yuksel M, et al. Lipid peroxidation and osmotic fragility of blood cells in sleep apnea patients, Clin Chim Acta.2003,332(1-2):83-88
13. Row B W, Liu R, Xu W, et al. Intermittent hypoxia is associated with oxidative stress and spatial learning deficits in the rat. Am J Respir Crit Care Med. 2003, 167:1548-1553.
14. Veasey S C, Davis C W, Fenik P, et al. Long-term Intermittent hypoxia in mice: protracted hypersomnolence with oxidative injury to sleep-wake brain regions.Sleep.2004, 27:194-201.
15. Gopalakrishnan A, Ji L L, Cirelli C. Sleep deprivation and cellular response to oxidative stress. Sleep. 2004, 27: 27-35.
16. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med. 2000, 162:566-570.
17. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med. 2002, 165:934-939.
18. Yokoyama M. Oxidative stress and atherosclerosis. Curr Opin Pharmacol. 2004, 4(2):110-115.
2. Alzoghaibi M A, Bahammam A S. Lipid peroxides,superoxide dismutase and circulating IL-8 and GCP-2 in patients with sivere obstructive sleep apnea: a pilot study. Sleep Breath. 2005, 9: 119-126.
3. Ozturk L, Mansour B, Yuksel M, et al. Lipid peroxidation and osmotic fragility of blood cells in sleep apnea patients, Clin Chim Acta.2003,332(1-2):83-88
4. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med. 2000, 162:566-570.
5. Macmillan Crow LA, Crow JP, Thompson JA. Peroxynitrite-mediated inactireation of manganese superoxide dismutase involves nitration and oxidation of critical tyrosine residues. Biochemistry. 1998, 37:1613-1622.
6. Christou K, Markoulis N,Moulas AN, et a1. Reactive oxygen metabolites(ROMs) as an index of oxidative stress in obstructive sleep apnoea patients. Sleep Breath.2003, 7(3):105-110.
7. Lavie L, Vishnevsky A , Lavie P. Evidence for lipid peroxidation in obstructive sleep apnea. Sleep. 2004, 27(1):123—128.
8. Barcelo A, Miralles C, Barbe F, et al.Abnormal lipid peroxidation in patients with sleep apnea. Eur Respir J.2000, 16: 644–647.
9. Yamauchi M, Nakano H, Maekawa J, et al. Oxidative stress in obstructive sleep apnea. Chest, 2005,127:1647-1679.
10. Nanduri R, Prabhakar PHD. Sleep apnea: an oxidative stress?. Am J Respir Crit Care Med, 2002, 165(7):859—860.
11. Carpagnano GE, Kharitonov SA, Resta O, et al. Increased 8-isoprostane and ynterleukin-6 in breath condensate of obstructive sleep apnea patients. Chest, 2002, 122(4): 1162-1167.
12. 张红,乔华,王广发.阻塞性睡眠呼吸暂停低通气综合征患者呼出凝集气过氧化氢浓度.中华结核和呼吸杂志.2006,29(8):541-544.
13. A.Barcelo, F.Barbe, M.de la pena, et al. Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment. Eur Respir J.2006, 27:756-760.
14. Kostas Christou, Anargyros N Moulas, Chaido Pastaka, et al. Antioxdant capacity in obstructive sleep apnoea patients. Sleep Med. 2003,4:225-228.
15. 汤树海,潘晓军. 阻塞性睡眠呼吸暂停综合征患者体内氧自由基代谢的作用.山东大学学报(医学版).2006, 44(5)
16. 温燕,李家树,宋满景. 阻塞性睡眠呼吸暂停低通气综合征患者体内氧化应激状态的分析.中国实用医药.2007, 2(22): 20-22.
17. Gopalakrishnan A, Ji L L, Cirelli C. Sleep deprivation and cellular response to oxidative stress. Sleep. 2004, 27: 27-35.
18. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med. 2002, 165:934-939.
19. Robinson GR, Stradling JR, Davies RJ. Sleep 6: obstructive sleep apnoea/hypopnoea syndrome and hypertention. Thorax. 2004,59(12):1089-1094.
20. Chobanian AV, Bakris GI, Black HR, et al. the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003,289(19):2560-2572.
21. Griendling KK, FitzGerald GA.Oxidative stress and cardiorascular injury : Part I: Basic mechanisms and in vivo mornitoring of ROS. Circulation. 2003,108(17):1912-1916.
22. Peker Y, Hedner J, Norum J, et al. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow up. Am J Respir Crit Care Med. 2002,166(2):159-165.
23. Mooe T, Franklin KA, Holmstrom K, et al. Sleep-disordered breathing and coronary artery disease: long-term prognosis. Am J Respir Crit Care Med. 2001,164(10): 1910-1913.
1. Christou K, Markoulis N,Moulas AN, et a1. Reactive oxygen metabolites(ROMs) as an index of oxidative stress in obstructive sleep apnoea patients. Sleep Breath.2003, 7(3):105-110.
2. Lavie L, Vishnevsky A , Lavie P. Evidence for lipid peroxidation in obstructive sleep apnea. Sleep. 2004, 27(1):123—128.
3. Barcelo A, Miralles C, Barbe F, et al.Abnormal lipid peroxidation in patients with sleep apnea. Eur Respir J.2000, 16: 644–647.
4. Yamauchi M, Nakano H, Maekawa J, et al. Oxidative stress in obstructive sleep apnea. Chest, 2005,127:1647-1679.
5. Nanduri R, Prabhakar PHD. Sleep apnea: an oxidative stress?. Am J Respir Crit Care Med, 2002, 165(7):859—860.
6. Carpagnano GE, Kharitonov SA, Resta O, et al. Increased 8-isoprostane and ynterleukin-6 in breath condensate of obstructive sleep apnea patients. Chest, 2002, 122(4): 1162-1167.
7. 张红,乔华,王广发.阻塞性睡眠呼吸暂停低通气综合征患者呼出凝集气过氧化氢浓度.中华结核和呼吸杂志.2006,29(8):541-544.
8. A.Barcelo, F.Barbe, M.de la pena, et al. Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment. Eur Respir J.2006, 27:756-760.
9. Kostas Christou, Anargyros N Moulas, Chaido Pastaka, et al. Antioxdant capacity in obstructive sleep apnoea patients. Sleep Med. 2003,4:225-228.
10. Svatikova A, Wolk R, Lerman L O, et al. Oxidative stress in obstructive sleep apnoea. Eur J Heart. 2005, 26:2435-2439.
11. Alzoghaibi M A, Bahammam A S. Lipid peroxides,superoxide dismutase and circulating IL-8 and GCP-2 in patients with sivere obstructive sleep apnea: a pilotstudy. Sleep Breath. 2005, 9: 119-126.
12. Ozturk L, Mansour B, Yuksel M, et al. Lipid peroxidation and osmotic fragility of blood cells in sleep apnea patients, Clin Chim Acta.2003,332(1-2):83-88
13. Row B W, Liu R, Xu W, et al. Intermittent hypoxia is associated with oxidative stress and spatial learning deficits in the rat. Am J Respir Crit Care Med. 2003, 167:1548-1553.
14. Veasey S C, Davis C W, Fenik P, et al. Long-term Intermittent hypoxia in mice: protracted hypersomnolence with oxidative injury to sleep-wake brain regions.Sleep.2004, 27:194-201.
15. Gopalakrishnan A, Ji L L, Cirelli C. Sleep deprivation and cellular response to oxidative stress. Sleep. 2004, 27: 27-35.
16. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med. 2000, 162:566-570.
17. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med. 2002, 165:934-939.
18. Yokoyama M. Oxidative stress and atherosclerosis. Curr Opin Pharmacol. 2004, 4(2):110-115.