Treatment of obstructive sleep apnoea leads to improved microvascular endothelial function in the systemic circulation

Treatment of obstructive sleep apnoea leads to improved microvascular endothelial function in the systemic circulation
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DOI:
10.1136/thx.2004.039164
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发表时间:
2006-06-01
期刊:
影响因子:
10
通讯作者:
Celermajer, DS
Celermajer, DS
中科院分区:
医学1区
文献类型:
--
作者:
Lattimore, JL;Wilcox, I;Celermajer, DS

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背景:阻塞性睡眠呼吸暂停(OSA)是一种常见的和潜在的可逆的原因,全身性高血压。然而,OSA导致高血压的机制以及治疗对动脉功能的影响尚未完全确定。在持续气道正压通气(CPAP)治疗前后对OSA患者的微血管动脉内皮和平滑肌功能进行了评估。方法:10名平均(SE)年龄49(8)岁的至少中度重度OSA患者在CPAP治疗前后3个月进行了详细的前臂血管反应性研究。通过测量肱动脉对动脉内注入乙酰胆碱的压力、流量和阻力反应来评估体循环(ACh;内皮依赖性血管扩张剂),硝普钠(SNP;内皮非依赖性血管扩张剂),L-NMMA(一氧化氮(NO)拮抗剂)和L-精氨酸结果:CPAP前,ACh和SNP均能剂量依赖性地增加前臂血流量(p < 0.01)。CPAP后,ACh的内皮依赖性舒张功能显著增加(CPAP后为基线的434(23)%,CPAP前为278(20)%,p < 0.001),而SNP诱导的舒张功能无变化。CPAP后静息NO产生更高,L-NMMA显著降低基础流量证明了这一点(p = 0.05)。结论:在OSA患者中,CPAP治疗可改善基线内皮NO释放,并刺激体循环中内皮依赖性血管舒张。这是CPAP治疗OSA患者改善全身和血管功能的潜在机制。
Background: Obstructive sleep apnoea (OSA) is a common and potentially reversible cause of systemic hypertension. The mechanisms whereby OSA leads to hypertension and the effects of treatment on arterial function, however, are not well established. Microvascular arterial endothelial and smooth muscle function was assessed in subjects with OSA before and after treatment with continuous positive airways pressure (CPAP).Methods: Ten subjects of mean (SE) age 49 (8) years with at least moderately severe OSA had detailed forearm vascular reactivity studies before and after 3 months of CPAP treatment. The systemic circulation was assessed by measuring brachial artery pressure, flow and resistance responses to intra-arterial infusions of acetylcholine (ACh; an endothelium dependent vasodilator), sodium nitroprusside (SNP; an endothelium independent vasodilator), L-NMMA (a nitric oxide (NO) antagonist), and L-arginine (the substrate for NO).Results: Before CPAP, ACh and SNP infusions increased forearm blood flow in a dose dependent manner (p < 0.01). After CPAP, endothelium dependent dilation to ACh was significantly increased (434 (23)% of baseline after CPAP v 278 (20)% before CPAP, p < 0.001), whereas SNP induced dilation was unchanged. Resting NO production was higher after CPAP, evidenced by a significantly greater reduction in basal flow by L-NMMA (p = 0.05). L-Arginine reversed the effect of L-NMMA in all cases.Conclusion: In patients with OSA, treatment with CPAP improves baseline endothelial NO release and stimulates endothelium dependent vasorelaxation in the systemic circulation. This is a potential mechanism for improving systemic and vascular function in patients with OSA treated with CPAP.