Effects of Acoustic Stimulation on Cardiovascular Regulation During Sleep

Abstract

The interaction of wake-sleep states and acoustic stimulation on cardiovascular regulation was studied on rats implanted with electroencephalogram and electromyogram electrodes and an arterial catheter. Mild acoustic stimuli (1000 Hz, 90 dB, 50-ms beeps) were administered during Wakefulness (W), non-rapid eye movement (NREM) sleep and REM sleep and the changes induced in heart period (HP, ms) and mean arterial pressure (MAP, mmHg) were analyzed. Two 30-s sequences of beat-to-beat HP and MAP values were considered before (I) and after (II) acoustic stimulation, respectively. By the effect of stimulation, state-dependent stimulus-locked HP and MAP oscillations were observed, HP oscillations being grossly parallel to the MAP ones but delayed with respect to MAP in the ascending part only; HP and MAP spontaneous fluctuations (HP and MAP variability) increased in NREM and REM sleep (but not in W); HP vs MAP correlation coefficient increased in an algebraic sense. These results show that 1) acoustic stimulation primarily affects the peripheral resistance, and secondarily, through the baroreceptor reflex, HP, thereby increasing the impact of peripheral versus centrally driven autonomic influences on the heart; 2) in NREM sleep, heart excitability is higher than requested by the baroreflex function; 3) cardiac variability is increased by acoustic stimulation during sleep (but not in W); this, in addition to the effects of point 2, may favor cardiac arrhythmias in NREM sleep. Thus, mild acoustic stimuli not perturbing cardiovascular regulation during W may create a specific risk factor during sleep in pathophysiologic conditions.

Sleep-Dependent Changes in the Coupling Between Heart Period and Arterial Pressure in Newborn Lambs

“…This feature of cardiovascular regulation may partly underlie the low cardiovascular variability in quiet sleep. Our data in newborn lambs are in broad agreement with those previously obtained in adult rats, in which the correlation between HP and MAP at low frequencies was higher in quiet sleep than either in active sleep or in quiet wakefulness both in control conditions and when cardiovascular regulation was perturbed by acoustic stimuli presented during sleep (6). It is of interest that neither in adult rats (5) nor in newborn lambs (18) does the gain of the cardiac baroreflex change significantly among wake-sleep states.…”

“…exercise (3), defense reaction (4)], may induce parallel changes in heart rate and in systemic vascular resistance. In adult rats, baroreflex control of heart rate prevails in quiet sleep, whereas central commands prevail in active sleep (5,6). Although effects of central autonomic commands on heart rate and arterial pressure are similar in wakefulness and in active sleep, the cause of such commands is uncertain in the latter state.…”

“…We analyzed the relationship between HP and mean arterial pressure (MAP) in the time domain by computing a cross-correlation function between spontaneous fluctuations in the two variables. Linear correlation has been proved to be a powerful tool to evaluate the balance of central and baroreflex control of HP in adult rats (6). The crosscorrelation function allows a more complete description of the system under study, as it yields information on the correlation between two signals as a function of the time shift, i.e.…”

Sleep-dependent changes in the coupling between heart period and blood pressure in human subjects

“…In turn, the fluctuations of HP may alter cardiac output, eliciting pressure fluctuations that are negatively correlated with them. Central autonomic commands (15) cause opposite changes in HP and vascular resistance (13), thereby apparently enhancing this feed-forward interaction.In animal models, the pattern of coupling between HP and blood pressure suggests a variable contribution of central and baroreflex mechanisms to cardiovascular control in different wake-sleep states (33,34,39). The baroreflex contribution appears most prominent during quiet sleep in lambs (33) and during nonrapid-eye-movement sleep (NREMS) in rats (34,39).…”

State of the art paper The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology

“…The classification of neurocardiological disorders by Goldstein [1] is as follows: 1) Sympathetic disorders -diseases in which activation of the catecholamine system worsens an independent pathological state (coronary artery disease, arrhythmias as long QT syndrome, sudden death, heart failure (HF)) as well as diseases in which abnormal catecholaminergic function is etiologic (sympathetic neurocirculatory failure, hypertension, cardiac necrosis and cardiomyopathy), and 2) Vagally mediated disorders -both neurally mediated syncope (vasovagal syncope, carotid sinus hypersensitivity) and vagally mediated atrial fibrillation. Neural regulation of the CV system can be studied by using different techniques [2][3][4][5][6][7][8]. G protein related kinases (GRKs) exist in 7 isoforms -GRK 1-7.…”