Autonomic neural control of cerebral hemodynamics

Abstract

Despite the rich innervation of the cerebral vasculature by both sympathetic and parasympathetic nerves [1], the role of autonomic control in cerebral circulation and, particularly, cerebral hemodynamics is not entirely clear [2]. Previous animal studies have reported inconsistent results regarding the effects of electrical stimulation or denervation on cerebral blood flow (CBF), cerebral pressure-flow relationship, and cerebral vessel response to metabolic stimuli [3]- [5]. Moreover, with the advance of transcranial Doppler ultrasound (TCD), which yields accurate-measurements of CBF velocity (CBFV) with high time resolution [6], it has been found that in humans CBFV in the middle cerebral artery decreased substantially during lower body negative pressure (LBNP) and head-up tilt in the absence of systemic hypotension, which suggests the presence of cerebral vasoconstriction associated with augmented sympathetic nerve activity during orthostatic stress [7]. These observations were based on assessing static measures of cerebral circulation, i.e., mean values of artevial blood pressure (ABP) and CBF with a low time resolution.However, the dynamic nature of cerebral autoregulation has been revealed using TCD measurements, to examine both the CBFV response to experimentally induced ABP changes [8]-[10] and the dynamic relation between spontaneous beat-to-beat ABP and CBFV variations [11]-[14]. These latter studies have revealed that dynamic autoregulation during resting conditions is frequency dependent, with slow ABP changes being attenuated more effectively by the cerebrovascular bed [14]. In this context, autonomic control of dynamic cerebral autoregulation was studied more recently by examining the dynamic relation between beat-to-beat ABP and CBFV variations during autonomic ganglion blockade. Transfer function analysis revealed a significant increase in the gain between ABP and CBFV from 0.02 to 0.07 Hz, suggesting altered autoregulation and active autonomic control [15].The cerebrovascular bed is exquisitely sensitive to changes in arterial CO 2 [1]. Recent studies have shown that small, spontaneous fluctuations of arterial CO 2 tension around the mean, assessed by end-tidal CO 2 (P ETCO 2 ) measurements, have a significant effect on slow fluctuations of both CBFV [12], [16] as well as regional blood flow, assessed by blood oxygen level-dependent functional magnetic resonance imaging [17], [18]. Furthermore, it has been suggested that cerebral hemodynamics are characterized by nonlinearities, both on the basis of low coherence values between ABP and mean CBFV (MCBFV) below 0.07 Hz [14] and by exploring the use of linear autoregressive models and the presence of nonlinear dynamics [19]. Consequently, we and others have shown that nonlinear Volterra models and/or multivariate models that incorporate P ETCO 2 variability are able to explain a considerably larger fraction of CBFV variability [12] Methods Experimental MethodsTwelve healthy subjects (nine men) with a mean age of 29 ± 6 years, height of 174 ± 10 cm...

Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

“…It must be appreciated that factors other than arterial blood gas tensions are known to modulate the effectiveness of dCA, these include: (i) sympathetic activity; (ii) metabolite production; and (iii) perivascular innervation [35][36][37][38][39][40]. Our data do not allow us to comment on the role that these factors played in disrupting autoregulatory processes during maximal apnoea.…”

Time-Varying Modeling of Cerebral Hemodynamics

“…These models include implicitly the effects of the myogenic mechanism [21], [22], flow-mediated endothelial mechanisms [23] and perivascular innervation [24]–[26] without yet being able to draw a direct correspondence between physiological mechanisms and specific model characteristics. Such input-output models often incorporate end-tidal CO2 measurements to account for the known effects of blood CO2 tension on this physiological process, especially in the low-frequency range from 0.02 to 0.08 Hz [8], [10], [12], [27]–[31]. Previous studies have shown that the characteristics of CFA and CVR are altered by orthostatic stress, hypertension, hypoxia, hypercapnia, head injury, stroke, early Alzheimer’s disease and pharmaceutical interventions that affect the autonomic nervous system or vascular tone [11], [12], [28], [32]–[38].…”

“…Such input-output models often incorporate end-tidal CO2 measurements to account for the known effects of blood CO2 tension on this physiological process, especially in the low-frequency range from 0.02 to 0.08 Hz [8], [10], [12], [27]–[31]. Previous studies have shown that the characteristics of CFA and CVR are altered by orthostatic stress, hypertension, hypoxia, hypercapnia, head injury, stroke, early Alzheimer’s disease and pharmaceutical interventions that affect the autonomic nervous system or vascular tone [11], [12], [28], [32]–[38]. Some of the recent findings were made possible by Volterra-type nonlinear modeling with two inputs (arterial blood pressure and end-tidal CO2) [10]–[12].…”

Orthostatic hypotension in dementia with Lewy bodies

“…Состо-яние мозгового кровотока модулируется не только церебральной ауторегуляцией, но и вегетативной нервной системой и артериальным барорефлектор-но-опосредованным контролем в большом круге кровообращения [41]. В ответ на симпатическую ак-тивацию наблюдается вазоконстрикция [42,43]. Це-ребральные механизмы ауторегуляции способны компенсировать потребление кислорода [44], одна-ко повторные эпизоды гипоперфузии приводят к истощению компенсаторных возможностей.…”