Katragadda S, Xie A, Puleo D, Skatrud J B, Morgan B J
Department of Medicine, University of Wisconsin, and Middleton Memorial Veterans Hospital, Madison, Wisconsin 53706, USA.
J Appl Physiol (1985). 1997 Dec;83(6):2048-54. doi: 10.1152/jappl.1997.83.6.2048.
Obstructive and nonobstructive apneas elicit substantial increases in muscle sympathetic nerve activity and arterial pressure. The time course of change in these variables suggests a causal relationship; however, mechanical influences, such as release of negative intrathoracic pressure and reinflation of the lungs, are potential contributors to the arterial pressure rise. To test the hypothesis that apnea-induced pressor responses are neurally mediated, we measured arterial pressure (photoelectric plethysmography), muscle sympathetic nerve activity (peroneal microneurography), arterial O2 saturation (pulse oximeter), and end-tidal CO2 tension (gas analyzer) during sustained Mueller maneuvers, intermittent Mueller maneuvers, and simple breath holds in six healthy humans before, during, and after ganglionic blockade with trimethaphan (3-4 mg/min, titrated to produce complete disappearance of sympathetic bursts from the neurogram). Ganglionic blockade abolished the pressor responses to sustained and intermittent Mueller maneuvers (-4 +/- 1 vs. +15 +/- 3 and 0 +/- 2 vs. +15 +/- 5 mmHg) and breath holds (0 +/- 3 vs. +11 +/- 3, all P < 0.05). We conclude that the acute pressor response to obstructive and nonobstructive voluntary apnea is sympathetically mediated.
阻塞性和非阻塞性呼吸暂停会引起肌肉交感神经活动和动脉压大幅升高。这些变量的变化时间进程表明存在因果关系；然而，诸如胸腔内负压释放和肺再充气等机械影响，是动脉压升高的潜在因素。为了验证呼吸暂停诱发的升压反应是由神经介导的这一假设，我们在六名健康受试者进行持续米勒动作、间歇性米勒动作和单纯屏气期间及之后，测量了动脉压（光电体积描记法）、肌肉交感神经活动（腓骨微神经图）、动脉血氧饱和度（脉搏血氧仪）和呼气末二氧化碳分压（气体分析仪），并在使用三甲噻芬（3 - 4毫克/分钟，滴定至神经图中交感神经爆发完全消失）进行神经节阻滞后重复测量。神经节阻滞消除了对持续和间歇性米勒动作（-4±1对+15±3和0±2对+15±5毫米汞柱）以及屏气（0±3对+11±3，所有P<0.05）的升压反应。我们得出结论，对阻塞性和非阻塞性自主呼吸暂停的急性升压反应是由交感神经介导的。
