中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
26期
1811-1814
,共4页
睡眠呼吸暂停,阻塞性%高血压%持续气道正压通气%醛固酮
睡眠呼吸暫停,阻塞性%高血壓%持續氣道正壓通氣%醛固酮
수면호흡잠정,조새성%고혈압%지속기도정압통기%철고동
Sleep apnea,obstructive%Hypertension%Continuous positive airway pressure%Aldosteronne
目的 探讨持续气道正压通气(CPAP)治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS)合并难治性高血压(RH)的疗效及其可能机制.方法 选择13例合并RH的中重度OSAHS患者,分别于CPAP治疗前及治疗3个月末测量睡前(22:00)、夜间(2:00)和清晨(6:00)的血压,并检测晨起(6:00)卧位血浆醛同酮(ALD)浓度和血浆肾素活性(PRA).ALD、PRA检测采用放射免疫分析法.结果 与CPAP治疗前相比,治疗第3个月末患者睡前、夜间和清晨血压(mm Hg,1 mm Hg=0.133 kPa)均显著下降(睡前135.5±2.8/84.2±4.6比152.2 4±19.2/98.9 4±15.6,夜间133.1 4±2.4/81.5 4±4.6比156.6 ±19.4/102.8±16.6,清晨151.5 ±3.0/81.2 4±3.2比172.1 ±23.7/98.1±6.5,均P<0.01);晨起卧位ALD浓度(pmoo/L)明显降低(411±54比542 ±43,P<0.01);但PRA(μg·L-1·h-1)无明显变化(0.27±0.14比0.204±0.12,P=0.221).结论 CPAP治疗可显著改善OSAHS合并RH患者的血压并降低血浆ALD浓度.OSAHS患者的RH可能与血浆ALD浓度增高有关.
目的 探討持續氣道正壓通氣(CPAP)治療阻塞性睡眠呼吸暫停低通氣綜閤徵(OSAHS)閤併難治性高血壓(RH)的療效及其可能機製.方法 選擇13例閤併RH的中重度OSAHS患者,分彆于CPAP治療前及治療3箇月末測量睡前(22:00)、夜間(2:00)和清晨(6:00)的血壓,併檢測晨起(6:00)臥位血漿醛同酮(ALD)濃度和血漿腎素活性(PRA).ALD、PRA檢測採用放射免疫分析法.結果 與CPAP治療前相比,治療第3箇月末患者睡前、夜間和清晨血壓(mm Hg,1 mm Hg=0.133 kPa)均顯著下降(睡前135.5±2.8/84.2±4.6比152.2 4±19.2/98.9 4±15.6,夜間133.1 4±2.4/81.5 4±4.6比156.6 ±19.4/102.8±16.6,清晨151.5 ±3.0/81.2 4±3.2比172.1 ±23.7/98.1±6.5,均P<0.01);晨起臥位ALD濃度(pmoo/L)明顯降低(411±54比542 ±43,P<0.01);但PRA(μg·L-1·h-1)無明顯變化(0.27±0.14比0.204±0.12,P=0.221).結論 CPAP治療可顯著改善OSAHS閤併RH患者的血壓併降低血漿ALD濃度.OSAHS患者的RH可能與血漿ALD濃度增高有關.
목적 탐토지속기도정압통기(CPAP)치료조새성수면호흡잠정저통기종합정(OSAHS)합병난치성고혈압(RH)적료효급기가능궤제.방법 선택13례합병RH적중중도OSAHS환자,분별우CPAP치료전급치료3개월말측량수전(22:00)、야간(2:00)화청신(6:00)적혈압,병검측신기(6:00)와위혈장철동동(ALD)농도화혈장신소활성(PRA).ALD、PRA검측채용방사면역분석법.결과 여CPAP치료전상비,치료제3개월말환자수전、야간화청신혈압(mm Hg,1 mm Hg=0.133 kPa)균현저하강(수전135.5±2.8/84.2±4.6비152.2 4±19.2/98.9 4±15.6,야간133.1 4±2.4/81.5 4±4.6비156.6 ±19.4/102.8±16.6,청신151.5 ±3.0/81.2 4±3.2비172.1 ±23.7/98.1±6.5,균P<0.01);신기와위ALD농도(pmoo/L)명현강저(411±54비542 ±43,P<0.01);단PRA(μg·L-1·h-1)무명현변화(0.27±0.14비0.204±0.12,P=0.221).결론 CPAP치료가현저개선OSAHS합병RH환자적혈압병강저혈장ALD농도.OSAHS환자적RH가능여혈장ALD농도증고유관.
Objective To investigate the efficacy and possible mechanism of continuous positive airway pressure (CPAP) therapy upon blood pressure in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and resistant hypertension (RH). Methods Thirteen OSAHS patients with RH were recruited. Before and after 3-month CPAP therapy, their blood pressures at 10:00 PM, 2:00 AM and 6:00 AM were measured and their morning plasma concentrations of aldosterone (ALD) and plasma renin activity (PRA) tested at supine position with radioimmunoassay. Results Compared with blood pressure parameters at pre-CPAP therapy, there was a significant decrease in blood pressure before sleep at the end of 3-month CPAP therapy [(135.5±2.8)/(84.2±4.6) vs (152.2 ±19.2)/(98.9 ± 15.6) mm Hg, P<0.01], at night during sleep [(133. 1± 2.4)/(81.5 ± 4.6) vs (156.6 ± 19.4)/(102.8 ± 16.6)mm Hg, P<0.01] and in the early morning [(151.5±3.0)/(81.2 ±3.2) vs (172.1±23.7)/(98.1 ±6.5) mm Hg, P <0.01]. Comparison of plasma concentrations of ALD and PRA before and after 3-month CPAP therapy indicated that there was a significant difference in ALD [(538±42) vs (408±53) pmol/L,0.221]. Conclusions CPAP therapy could significantly improve RH and plasma ALD concentration.Elevated plasma ALD concentration is possibly involved in the pathogenesis of RH in OSAHS patients.
