Patients with obstructive sleep apnea (OSA) experience repetitive nocturnal hemodynamic oscillations, with marked increases in arterial pressure at apnea termination. Over time, elevations of arterial pressure may contribute to acute and chronic cardiovascular disease, but the causes and immediate consequences of the arterial pressure fluctuations remain uncertain. Although attention has focused on hypoxia to account for the pressure elevations, over the last three years we have acquired data to support an alternative hypothesis. We hypothesize that arousal, the sudden disruption of sleep architecture, is primarily responsible for the acute hemodynamic response to upper airway obstruction during sleep. However, recent investigations of OSA patients sleeping without obstructions on nasal continuous positive airway pressure suggest that the hemodynamic response to arousal is superimposed on an already abnormally elevated arterial pressure. To explain this abnormal increase in pressure even during uninterrupted sleep, we hypothesize that control of hemodynamic function during sleep (with or without interruption) is abnormal in OSA patients. Furthermore, we hypothesize that this abnormal hemodynamic function is due, in part, to abnormal reflex control mechanisms. To test these hypotheses in the current proposal, we plan further studies to define the specific mechanisms that account for the post-apnea increase in arterial pressure. During the proposed project we will also define the hemodynamic/sympathetic neural changes that occur during uninterrupted sleep in OSA patients. Finally, we will begin to determine the contribution of abnormal reflex control mechanisms to arterial pressure regulation during sleep in patients and normals. We are particularly interested in the relationships among nocturnal arterial pressure, cardiac output, systemic vascular resistance, forearm vascular resistance and muscle sympathetic nerve activity. We will attempt to define the complex hemodynamic events of sleep with and without obstructions, using vascular pressure measurements, nuclear cardiography, forearm venous plethysmography, skin laser velocimetry, and peroneal microneurography. These investigations will add to our understanding of the extreme elevations of arterial pressure experienced during sleep by patients with OSA.
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