Cortical regions associated with autonomic cardiovascular regulation during lower body negative pressure in humans

Abstract

The purpose of the present study was to determine the cortical structures involved with integrated baroreceptor-mediated modulation of autonomic cardiovascular function in conscious humans independent of changes in arterial blood pressure. We assessed the brain regions associated with lower body negative pressure (LBNP)-induced baroreflex control using functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast in eight healthy male volunteer subjects. The levels of LBNP administered were 5, 15 and 35 mmHg. Heart rate (HR; representing the cardiovascular response) and LBNP (representing the baroreceptor activation level) were simultaneously monitored during the scanning period. In addition, estimated central venous pressure (CVP), arterial blood pressure (ABP) and muscle sympathetic nerve activity were recorded on a separate session. Random effects analyses (SPM2) were used to evaluate significant (P < 0.05) BOLD signal changes that correlated separately with both LBNP and HR (15-and 35-mmHg versus 5-mmHg LBNP). Compared to baseline, steady-state LBNP at 15 and 35 mmHg decreased CVP (from 7 ± 1 to 5 ± 1 and 4 ± 1 mmHg, respectively) and increased MSNA (from 12 ± 1 to 23 ± 3 and 36 ± 4 bursts min −1 , respectively, both P < 0.05 versus baseline). Furthermore, steady-state LBNP elevated HR from 54 ± 2 beats min −1 at baseline to 64 ± 2 beats min −1 at 35-mmHg suction. Both mean arterial and pulse pressure were not different between rest and any level of LBNP. Cortical regions demonstrating increased activity that correlated with higher HR and greater LBNP included the right superior posterior insula, frontoparietal cortex and the left cerebellum. Conversely, using the identical statistical paradigm, bilateral anterior insular cortices, the right anterior cingulate, orbitofrontal cortex, amygdala, midbrain and mediodorsal nucleus of the thalamus showed decreased neural activation. These data corroborate previous investigations highlighting the involved roles of the insula, anterior cingulate cortex and amygdala in central autonomic cardiovascular control. In addition, we have provided the first evidence for the identification of the cortical network involved specifically with baroreflex-mediated autonomic cardiovascular function in conscious humans.

Brain correlates of autonomic modulation: Combining heart rate variability with fMRI

“…However, when the methodology reported by Critchley et al was applied to our own data, no brain regions passed an identical post-processing threshold cutoff used for our methodology. Other studies have attempted to correlate HR or MAP with fMRI (Kimmerly et al 2005) or PET (Critchley et al 2000). However, measures such as mean heart rate (or mean RR interval) do not proportionally quantify either sympathetic or parasympathetic modulation (Malik et al 1996), and are thus less likely to relate to activity in discrete brain regions with known sympathetic or parasympathetic connections.…”

Effect of Parasympathetic Stimulation on Brain Activity During Appraisal of Fearful Expressions

“…Many of these brain centers are implicated in autonomic regulation (Critchley, 2005a;Kimmerly et al, 2005). In a previous study, our group used the same methodology to describe the modulation by CS of activity within regions, including insula, amygdala, and PAG, both at rest and when participants were engaged in a cognitive task (Basile et al, 2013a), or during processing of sad, happy, angry, and neutral faces (Basile et al, 2013b).…”

O Volume De Exercícios Resistidos Influencia a Reatividade Da Pressão Arterial Ao Estresse

“…A HA tem sido associada com uma aumentada reatividade vascular durante e após períodos agudos de estresse induzido 6,7 . Estudos anteriores 8,9 evidenciaram aumentos no débito cardíaco, na vasoconstricção, na resistência vascular periférica, na atividade nervosa simpática e, por conseguinte, elevações anormais na pressão arterial em humanos que se encontravam em condições de estresse.…”

“…O exercício físico pode promover aumento os níveis circulantes de endorfinas [5][6][7][8][9][10][11][12] , aumento da atividade autonômica parassimpática em repouso e períodos de recuperação pós-exercícios 12 , bem como, diminuição das concentrações séricas e locais de noradrenalina 2 e aumento da biodisponibilidade de óxido nítrico. Ullman et al 13 , demostraram que indiví-duos normotensos com hiper-reatividade da pressão arterial ao estresse, quando submetidos a um programa de treinamento aeróbio, reduzem seus níveis pressóricos em resposta a um teste de estresse cardiovascular.…”

“…Pelo que temos conhecimento, apenas um estudo realizado especificamente com exercício resistido investigou respostas de pressão arterial ao estresse cardiovascular induzido 8 . Nesse estudo não foram identificadas alterações significativas na reatividade vascular, contudo, o exercício foi realizado com isometria.…”