NEURAL MECHANISM OF THE PRESSOR-RESPONSE TO OBSTRUCTIVE AND NONOBSTRUCTIVE APNEA

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.