Hypoxia-mediated prolonged elevation of sympathetic nerve activity after periods of intermittent hypoxic apnea
Hypoxia-mediated prolonged elevation of sympathetic nerve activity after periods of intermittent hypoxic apnea
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DOI：
10.1152/japplphysiol.00506.2003
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发表时间：
2004-02-01
影响因子：
3.3
通讯作者：
Smith, ML
中科院分区：
文献类型：
--
作者：
Cutler, MJ;Swift, NM;Smith, ML
阻塞性睡眠呼吸暂停（OSA）与呼吸暂停事件期间肌肉交感神经活动（MSNA）的短暂升高有关，这通常会导致OSA患者白天MSNA升高。缺氧被认为是OSA患者白天MSNA升高的主要刺激因素。因此，我们研究了20分钟的间歇性自主低氧呼吸暂停对MSNA在180分钟的恢复。此外，我们比较了间歇性自主低氧性呼吸暂停、高碳酸性低氧或等碳酸性低氧20分钟后恢复期间的MSNA。与我们的假设相一致，在间歇性低氧性呼吸暂停20分钟后，总MSNA和MSNA爆发频率与基线相比均升高（P < 0.05）。总MSNA和MSNA爆发频率在整个180分钟恢复期内保持升高，并且在整个该期间与时间对照受试者具有统计学差异（P < 0.05）。最后，从间歇性低氧性呼吸暂停、高碳酸性低氧和等碳酸性低氧恢复期间的MSNA没有差异（P = 0.50）。因此，这些数据支持以下假设：短期暴露于间歇性低氧性呼吸暂停导致MSNA持续升高，低氧是这种反应的主要介质。
Obstructive sleep apnea (OSA) is associated with transient elevation of muscle sympathetic nerve activity (MSNA) during apneic events, which often produces elevated daytime MSNA in OSA patients. Hypoxia is postulated to be the primary stimulus for elevated daytime MSNA in OSA patients. Therefore, we studied the effects of 20 min of intermittent voluntary hypoxic apneas on MSNA during 180 min of recovery. Also, we compared MSNA during recovery after either 20 min of intermittent voluntary hypoxic apneas, hypercapnic hypoxia, or isocapnic hypoxia. Consistent with our hypothesis, both total MSNA and MSNA burst frequency were elevated after 20 min of intermittent hypoxic apnea compared with baseline ( P < 0.05). Both total MSNA and MSNA burst frequency remained elevated throughout the 180-min recovery period and were statistically different from time control subjects throughout this period ( P < 0.05). Finally, MSNA during recovery from intermittent hypoxic apnea, hypercapnic hypoxia, and isocapnic hypoxia were not different ( P = 0.50). Therefore, these data support the hypothesis that short-term exposure to intermittent hypoxic apnea results in sustained elevation of MSNA and that hypoxia is the primary mediator of this response.