Ventilatory and cardiovascular responses to hypercapnia and hypoxia in multiple-system atrophy.
BACKGROUND
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.


OBJECTIVE
To determine whether ventilatory and cardiovascular responses to hypercapnia and hypoxia during wakefulness are systematically impaired in MSA.


METHODS
Case-control study.


METHODS
Mayo Clinic, Rochester, Minnesota.


METHODS
Sixteen patients with probable MSA (cases) and 14 age-matched control subjects (controls).


METHODS
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.


RESULTS
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).


CONCLUSIONS
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.
Lipp
Axel
A
Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Schmelzer
James D
JD
Low
Phillip A
PA
Johnson
Bruce D
BD
Benarroch
Eduardo E
EE
D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000209:etiology; D001794:Blood Pressure / Q000502:physiology*; D016022:Case-Control Studies; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D006935:Hypercapnia / Q000209:etiology*; D007024:Hypotension, Orthostatic / Q000209:etiology; D000860:Hypoxia / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D019578:Multiple System Atrophy / Q000150:complications*; D012123:Pulmonary Ventilation / Q000502:physiology*; D018709:Statistics, Nonparametric