Lipp Axel, Schmelzer James D, Low Phillip A, Johnson Bruce D, Benarroch Eduardo E
Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Arch Neurol. 2010 Feb;67(2):211-6. doi: 10.1001/archneurol.2009.321.
Loss of medullary sympathoexcitatory neurons may contribute to baroreflex failure, leading to orthostatic hypotension in multiple-system atrophy (MSA). The cardiovascular responses to chemoreflex activation in MSA have not been explored to date.
To determine whether ventilatory and cardiovascular responses to hypercapnia and hypoxia during wakefulness are systematically impaired in MSA.
Case-control study.
Mayo Clinic, Rochester, Minnesota.
Sixteen patients with probable MSA (cases) and 14 age-matched control subjects (controls).
Minute ventilation, blood pressure, and heart rate responses to hypercapnia and hypoxia during wakefulness. Hypercapnia was induced by a rebreathing technique and was limited to a maximal expiratory partial pressure of carbon dioxide of 65 mm Hg. Hypoxia was induced by a stepwise increase in inspiratory partial pressure of nitrogen and was limited to a minimal arterial oxygen saturation of 80%. Ventilatory responses were assessed as slopes of the regression line relating minute ventilation to changes in arterial oxygen saturation and partial pressure of carbon dioxide.
In cases, ventilatory responses to hypercapnia and hypoxia were preserved, despite the presence of severe autonomic failure, while cardiovascular responses to these stimuli were impaired. Among cases, hypercapnia elicited a less robust increase in arterial pressure than among controls, and hypoxia elicited a depressor response rather than the normal pressor responses (P < .001 for both).
Ventilatory responses to hypercapnia and hypoxia during wakefulness may be preserved in patients with MSA, despite the presence of autonomic failure and impaired cardiovascular responses to these stimuli. A critical number of chemosensitive medullary neurons may need to be lost before development of impaired automatic ventilation during wakefulness in MSA, whereas earlier loss of medullary sympathoexcitatory neurons may contribute to the impaired cardiovascular responses in these patients.
延髓交感神经兴奋神经元的丧失可能导致压力反射衰竭，进而引发多系统萎缩（MSA）患者的体位性低血压。迄今为止，尚未对MSA患者化学反射激活后的心血管反应进行研究。
确定MSA患者在清醒状态下对高碳酸血症和低氧血症的通气及心血管反应是否存在系统性损害。
病例对照研究。
明尼苏达州罗切斯特市的梅奥诊所。
16例可能患有MSA的患者（病例组）和14例年龄匹配的对照受试者（对照组）。
清醒状态下对高碳酸血症和低氧血症的分钟通气量、血压及心率反应。高碳酸血症通过重复呼吸技术诱发，将呼气末二氧化碳分压的最大值限制在65 mmHg。低氧血症通过逐步增加吸入氮气分压诱发，将动脉血氧饱和度的最小值限制在80%。通气反应通过将分钟通气量与动脉血氧饱和度及二氧化碳分压变化相关的回归线斜率进行评估。
在病例组中，尽管存在严重的自主神经功能衰竭，但对高碳酸血症和低氧血症的通气反应仍得以保留，而对这些刺激的心血管反应则受损。在病例组中，与对照组相比，高碳酸血症引起的动脉压升高幅度较小，低氧血症引起的是降压反应而非正常的升压反应（两者P均<0.001）。
尽管存在自主神经功能衰竭且对这些刺激的心血管反应受损，但MSA患者在清醒状态下对高碳酸血症和低氧血症的通气反应可能得以保留。在MSA患者清醒状态下出现自动通气受损之前，可能需要丧失一定数量的化学敏感延髓神经元，而延髓交感神经兴奋神经元的早期丧失可能导致这些患者的心血管反应受损。
