S. Katragadda et al., NEURAL MECHANISM OF THE PRESSOR-RESPONSE TO OBSTRUCTIVE AND NONOBSTRUCTIVE APNEA, Journal of applied physiology, 83(6), 1997, pp. 2048-2054
Obstructive and nonobstructive apneas elicit substantial increases in
muscle sympathetic nerve activity and arterial pressure. The time cour
se of change in these variables suggests a causal relationship; howeve
r, mechanical influences, such as release of negative intrathoracic pr
essure and reinflation of the lungs, are potential contributors to the
arterial pressure rise. To test the hypothesis that apnea-induced pre
sser responses are neurally mediated, we measured arterial pressure (p
hotoelectric plethysmography), muscle sympathetic nerve activity (pero
neal microneurography), arterial O-2 saturation (pulse oximeter), and
end-tidal CO2 tension (gas analyzer) during sustained Mueller maneuver
s, intermittent Mueller maneuvers, and simple breath holds in six heal
thy humans before, during, and after ganglionic blockade with trimetha
phan (3-4 mg/min, titrated to produce complete disappearance of sympat
hetic bursts from the neurogram). Ganglionic blockade abolished the pr
esser 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 pres
ser response to obstructive and nonobstructive voluntary apnea is symp
athetically mediated.