Hemodynamics and muscle sympathetic nerve activity after 8 h of sustained hypoxia in healthy humans.
Hemodynamics and muscle sympathetic nerve activity after 8 h of sustained hypoxia in healthy humans.
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健康人持续缺氧 8 小时后的血流动力学和肌肉交感神经活动。
DOI：
10.1152/ajpheart.00277.2007
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Weiss,JWoodrow
中科院分区：
文献类型：
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作者：
Tamisier,Renaud;Hunt,BrianE;Gilmartin,GeoffreyS;Curley,Mathew;Anand,Amit;Weiss,JWoodrow
对12名正常受试者在连续低氧8h前、中(1h和7h)和低氧机械习服后的血流动力学、肌交感神经活动(MSNA)和前臂血流量进行了测定。所有结果均为均值±标准差。受试者暴露期间的平均血氧饱和度为84.3±2.3%。暴露导致低氧习服，如呼气末二氧化碳[44.7±2.7(前)比39.5±2.2毫米汞柱(P<；0.001)]和对低氧的通气性反应[1.2±0.8(前)比2.3±1.3 L·分−1·1%下降饱和度−1(后)，P<；0.05]。与暴露前相比，受试者在暴露期间表现出显著的心率增加，即使在回到室内空气呼吸后仍保持较高的心率(67.3士15.9vs.59.8士12.1拍/分钟，P<；0.008)。尽管动脉压在整个暴露过程中显示出增加的趋势，但这并不显著。MSNA最初从室内空气到低氧时升高(2 6.2±10.3次/百次至32.0±10.3次/百次，暴露1h时不明显)；然而，尽管持续低氧(2 0.9±8.0次/百次/百次，7h Hx比1h Hx；P<；0.008)，MSNA仍降至常氧基线以下。在受试者回到室内空气中后，MSNA进一步降低(与基线相比，每百次心跳减少16.6±6.0ms；P<；0.008)。前臂电导由暴露前的2.9±1.5增至4.3±1.6(P<；0.01)。这些发现表明，在持续低氧8小时后，心血管和呼吸控制发生了变化，不仅产生了习服，而且产生了交感抑制。
Hemodynamics, muscle sympathetic nerve activity (MSNA), and forearm blood flow were evaluated in 12 normal subjects before, during (1 and 7 h), and after ventilatory acclimatization to hypoxia achieved with 8 h of continuous poikilocapnic hypoxia. All results are means ± SD. Subjects experienced mean oxygen saturation of 84.3 ± 2.3% during exposure. The exposure resulted in hypoxic acclimatization as suggested by end-tidal CO2[44.7 ± 2.7 (pre) vs. 39.5 ± 2.2 mmHg (post),P< 0.001] and by ventilatory response to hypoxia [1.2 ± 0.8 (pre) vs. 2.3 ± 1.3 l·min−1·1% fall in saturation−1(post),P< 0.05]. Subjects exhibited a significant increase in heart rate across the exposure that remained elevated even upon return to room air breathing compared with preexposure (67.3 ± 15.9 vs. 59.8 ± 12.1 beats/min,P< 0.008). Although arterial pressure exhibited a trend toward an increase across the exposure, this did not reach significance. MSNA initially increased from room air to poikilocapnic hypoxia (26.2 ± 10.3 to 32.0 ± 10.3 bursts/100 beats, not significant at 1 h of exposure); however, MSNA then decreased below the normoxic baseline despite continued poikilocapnic hypoxia (20.9 ± 8.0 bursts/100 beats, 7 h Hx vs. 1 h Hx;P< 0.008 at 7 h). MSNA decreased further after subjects returned to room air (16.6 ± 6.0 bursts/100 beats;P< 0.008 compared with baseline). Forearm conductance increased after exposure from 2.9 ± 1.5 to 4.3 ± 1.6 conductance units (P< 0.01). These findings indicate alterations of cardiovascular and respiratory control following 8 h of sustained hypoxia producing not only acclimatization but sympathoinhibition.