Hemodynamic effects of pressures applied to the upper airway during sleep

The increase in systemic blood pressure after an obstructive apnea is due, in part, to sympathetically mediated vasoconstriction. We questioned whethe r upper airway (UA) receptors could contribute reflexly to this vasoconstri ction. Four unanesthetized dogs were studied during wakefulness and non-rap id-eye-movement (NREM) sleep. The dogs breathed via a fenestrated tracheost omy tube sealed around the tracheal stoma. The snout was sealed with an air tight mask, thereby isolating the UA when the fenestration was closed and e xposing the UA to negative inspiratory intrathoracic pressure when it was o pen. The blood pressure response to three UA perturbations was studied: 1) square-wave negative pressures sufficient to cause UA collapse with the fen estration closed during a mechanical hyperventilation-induced central apnea ; 2) tracheal occlusion with the fenestration open vs. closed; and 3) high- frequency pressure oscillations (HFPO) with the fenestration closed. During NREM sleep, 1) blood pressure response to tracheal occlusion was similar w ith the fenestration open or closed; 2) collapsing the UA with negative pre ssures failed to alter blood pressure during a central apnea; and 3) applic ation of HFPO to the UA during eupnea and resistive-loaded breaths increase d heart rate and blood pressure. However, these changes were likely to be s econdary to the effects of HFPO-induced reflex changes on prolonging expira tory time. These findings suggest that activation of UA pressure-sensitive receptors does not contribute directly to the presser response associated w ith sleep-disordered breathing events.