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Effect of simulated obstructive hypopnea and apnea on thoracic aortic wall transmural pressures

机译:模拟梗阻性缺水和呼吸暂停对胸主动脉膜透射压力的影响

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Clarenbach CF, Camen G, Sievi NA, Wyss C, Stradling JR, Kohler M. Effect of simulated obstructive hypopnea and apnea on thoracic aortic wall transmural pressures. J Appl Physiol 115: 613-617, 2013. First published June 13, 2013; doi:10.1152/japplphysiol.00439.2013.-Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation, although potential causative mechanisms are incompletely understood; these may include an increase in aortic wall transmural pressures, induced by obstructive apneas and hypopneas. In patients undergoing cardiac catheterization, mean blood pressure (MBP) in the thoracic aorta and esophageal pressure was simultaneously recorded by an indwelling aortic pigtail catheter and a balloontipped esophageal catheter in randomized order during: normal breathing, simulated obstructive hypopnea (inspiration through a threshold load), simulated obstructive apnea (Mueller maneuver), and end-expiratory central apnea. Aortic transmural pressure (aortic MBP minus esophageal pressure) was calculated. Ten patients with a median age (range) of 64 (46 -75) yr were studied. Inspiration through a threshold load, Mueller maneuver, and end-expiratory central apnea was successfully performed and recorded in 10, 7, and 9 patients, respectively. The difference between aortic MBP and esophageal pressure (and thus the extra aortic dilatory force) was median (quartiles) +9.3 (5.4, 18.6) mmHg, P = 0.02 during inspiration through a threshold load, +16.3 (12.8, 19.4) mmHg, P = 0.02 during the Mueller maneuver, and +0.4 ( +4.5, 4.8) mmHg, P = 0.80 during end-expiratory central apnea. Simulated obstructive apnea and hypopnea increase aortic wall dilatory transmural pressures because intraaortic pressures fall less than esophageal pressures. Thus OSA may mechanically promote thoracic aortic dilatation and should be further investigated as a risk factor for the development or accelerated progression of thoracic aortic aneurysms.
机译:Clarenbach CF,Camen G,Sievi Na,Wyss C,Sharling JR,Kohler M.模拟阻塞性缺水和呼吸暂停对胸主动脉膜跨膜的影响。 J Ampl Physiol 115:613-617,2013。2013年6月13日第一次出版; DOI:10.1152 / japplphysiol.00439.2013.初步证据支持阻塞性睡眠呼吸暂停(OSA)和胸主动脉扩张之间的关联,尽管潜在的致病机制不完全理解;这些可以包括由阻塞性呼吸暂停和低钠诱导的主动脉膜跨膜压力的增加。在接受心脏导管插入术的患者中,胸主动脉和食管压力中的平均血压(MBP)在:在:正常呼吸,模拟阻塞性缺水期间,在随机顺序中同时记录胸部主动脉导管和气球食管导管的血压(MBP)。 ),模拟阻塞性呼吸暂停(Mueller机动)和末端呼气中央呼吸暂停。计算主动脉透气压力(主动脉染色体MBP减去食管压力)。研究了64(46-75)YR中位年龄(范围)的十名患者。通过阈值载荷,穆勒机动和末期呼气中央呼吸暂停的灵感分别在10,7和9名患者中成功进行和记录。主动脉MBP和食管压力之间的差异(以及额外的主动脉稀释力)是中值(四分气夹)+ 9.3(5.4,18.6)mmHg,通过阈值载荷,+ 16.3(12.8,19.4)mmHg, P = 0.02在穆勒机动期间,+ 0.4(+ 4.5,4.8)mmHg,末期呼气中央呼吸暂停期间P = 0.80。模拟阻塞性呼吸暂停和缺血性增加主动脉壁膨胀透射压力,因为内部压力落下小于食道压力。因此,OSA可以机械地促进胸主动脉扩张,并且应该进一步研究作为胸主动脉瘤的发育或加速进展的危险因素。

著录项

  • 来源
    《Journal of applied physiology 》 |2013年第5期| 共5页
  • 作者单位

    Sleep Disorders Center and Pulmonary Division University Hospital Zurich Raemistrasse 100 8091;

    Sleep Disorders Center and Pulmonary Division University Hospital Zurich Raemistrasse 100 8091;

    Sleep Disorders Center and Pulmonary Division University Hospital Zurich Raemistrasse 100 8091;

    Division of Cardiology University Hospital Zurich Zurich Switzerland;

    Oxford Center for Respiratory Medicine and Oxford Biomedical Research Centre Churchill Hospital;

    Sleep Disorders Center and Pulmonary Division University Hospital Zurich Raemistrasse 100 8091;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 人体生理学 ;
  • 关键词

    Aortic dilatation; Obstructive sleep apnea; Transmural aortic pressure;

    机译:主动脉扩张;阻塞性睡眠呼吸暂停;透透体压力;

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