Sympathetic baroreceptor regulation during hypoxic hypotension in humans: new insights.

Abstract

Baroreceptor activation by a continuous infusion of phenylephrine selectively abolishes the muscle sympathetic nerve activity (MSNA) response to hypoxia in humans. Baroreceptor deactivation enhances the MSNA rise during hypoxia in animals. Whether this is true in humans is unknown and was tested in the present study. We assessed MSNA responses elicited by isocapnic hypoxia (10% O2 in N2) during baroreflex loading and unloading with phenylephrine and nitroprusside, respectively, in 19 healthy volunteers. The study was randomized and placebo-controlled. Phenylephrine and nitroprusside increased and decreased, respectively, blood pressure during normoxia and hypoxia, whereas the reverse occurred for heart rate and MSNA (all P < 0.001 vs. placebo). As compared with normoxia, cardiac barosensitivity decreased during the infusion of placebo and nitroprusside in the presence of hypoxia, as well as sympathetic barosensitivity during the infusion of nitroprusside (all P < 0.05). Three patients even disclosed a reduction in arterial pressure, which became apparent at the third minute of hypoxia and worsened steadily thereafter (SBP: 91 ± 7 mmHg; DBP 47 ± 9 mmHg), in spite of a gradual rise in heart rate of 20 ± 4 bpm. Changes in baroreceptor loading conditions did not affect ventilation during normoxia and hypoxia. Cardiac and sympathetic baroreceptor sensitivity decrease during baroreceptor unloading in the presence of peripheral chemoreceptor activation. Normal humans have limited reflex capabilities to sustain simultaneous reductions in oxygen and pressure, and may experience hemodynamic instability episodes in such condition.