Why the study?
Does obstructive apnea during sleep cause peripheral vasoconstriction in patients with obstructive sleep apnea syndrome?
Does obstructive apnea during sleep cause peripheral vasoconstriction in patients with obstructive sleep apnea syndrome?
Obstructive apneas in sleep apnea syndrome cause transient limb vasoconstriction that is mediated by the sympathetic nervous system and linked to hypoxia.
Supports sympathetic mediation of postapneic vasoconstriction in OSA; leaves open long-term CV risk implications.
Obstructive apnea during sleep is associated with a substantial transient blood pressure elevation. The mechanism of this pressor response is unclear. In this study we measured muscle sympathetic nerve activity (MSNA), mean arterial pressure (Psa), and mean limb blood velocity as an index of blood flow (MBV, Doppler) and calculated changes in limb vascular resistance during and after apneas during both wakefulness and sleep in patients with the obstructive sleep apnea syndrome. Immediately postapnea during sleep Psa increased significantly compared with the earlier stages of apnea and this was preceded by a rise of MSNA (n = 5). In contrast to blood pressure, MBV remained unchanged. Because resistance = blood pressure/blood flow, limb vascular resistance increased by 29 +/- 8% from late apnea to postapnea (n = 7, p < 0.002). Voluntary breathhold maneuvers during room air exposure evoked similar responses (n = 10). Supplemental oxygen administered via nonrebreather face mask attenuated the MSNA and vasoconstrictor responses to obstructive (n = 2) and voluntary apneas (n = 10). Our data suggest that obstructive apneas in patients with the obstructive apnea syndrome are accompanied by transient limb vasoconstriction. This vasoconstrictor response appears to be, at least in part, mediated by the sympathetic nervous system and may be linked to hypoxia.
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Imadojemu et al. (2002) studied this question.
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