Sleep and the Peripheral Vascular System

Abstract

During sleep as during wakefulness, cardiovascular regulation acts to guarantee an adequate blood flow (BF) supply to body organs, in particular the brain and the heart, the metabolic requirements of which vary with the behavioral states of the wake–sleep cycle. In the brain, flow-activity coupling produces cerebral BF changes on a regional basis: cerebral BF decreases during non-rapid eye movement (NREM) sleep compared with previous wakefulness mainly in regions involved in the generation of sleep itself, of δ-activity, or in the modulation of cortical activation. During rapid eye movement (REM) sleep, cerebral BF tonically increases with respect to NREM sleep, particularly in areas important for REM sleep generation and in regions potentially involved in emotional memory processing. These sleep-dependent differences in cerebral BF mainly depend on nitric oxide signaling. Evidence that sleep-dependent changes in spinal cord BF parallel those in cerebral BF suggests that sleep modulates the activity of the central nervous system as a whole. Sleep-dependent changes in coronary BF also closely parallels the changes in myocardial tissue metabolism. A decrease in coronary BF occurs during NREM sleep with respect to previous wakefulness, while during REM sleep, coronary BF not only returns tonically to wakefulness levels, but also undergoes phasic surges, coupled with bursts of sinus tachycardia. BF to most skeletal muscle groups varies as a consequence of a progressive reduction of muscle activity on passing from wakefulness to NREM sleep and then to REM sleep. Muscle BF is thus lower during sleep, and particularly during REM sleep, than during wakefulness. In other peripheral beds, BF changes during sleep depend in part on thermoregulatory processes. Thus, cutaneous vasodilation during sleep helps to dissipate body heat because of a decreased body temperature set point, while the impairment of thermoregulatory processes in REM sleep produces paradoxical changes in skin BF in presence of a thermal challenge. Renal and splanchnic vascular beds also play a role in the integrated pattern of thermoregulatory vasomotor adjustments. The disruption of this pattern during REM sleep causes a drop in sympathetic vasomotor tone, increasing splanchnic and renal BF with respect to NREM sleep, both at low and high ambient temperatures. During REM sleep, sympathetic outflow to different vascular beds is highly heterogeneous even in the absence of thermal loads, suggesting the existence of a central repatterning of sympathetic activity specific of this sleep stage. The physiological hemodynamic changes that occur in normal subjects during sleep may be deeply affected by sleep-related pathological conditions, such as obstructive sleep apnea, or by sleep loss.