Literature DB >> 19363133

Lateralization of expression of neural sympathetic activity to the vessels and effects of carotid baroreceptor stimulation.

André Diedrich1, Alberto Porta, Franca Barbic, Robert J Brychta, Pietro Bonizzi, Laura Diedrich, Sergio Cerutti, David Robertson, Raffaello Furlan.   

Abstract

Human studies suggest that cardiovascular neural sympathetic control is predominantly modulated by the right cerebral hemisphere. It is unknown whether post-ganglionic sympathetic activity [muscle sympathetic nerve activity (MSNA)] shows any functional asymmetry. Eight right-handed volunteers (3 women and 5 men, 32 +/- 2 yr of age) underwent ECG, beat-by-beat blood pressure, respiratory activity, and simultaneous right and left MSNA recordings during spontaneous and controlled breathing (CB, 15 breaths/min, 0.25 Hz). Dynamic carotid baroreceptor stimulation was obtained by 0.1-Hz sinusoidal suction, from 0 to -50 mmHg, randomly applied to the right, left, and combined right and left sides of the neck during CB. Laterality was assessed by changes in the MSNA burst rate (in bursts/min, and bursts/100 beats), strength [amplitude (A) and area (AA)], and the oscillatory component at 0.1 Hz during baroreceptor stimulation. Amplitude parameters were normalized by CB burst mean amplitude and area of the same side. At rest, the right and left MSNA burst rate and total MSNA activity were similar. Conversely, the right MSNA normalized burst A(N) (1.36 +/- 0.18) and AA(N) (1.31 +/- 0.16) were larger than the left MSNA A(N) (1.04 +/- 0.09) and AA(N) (1.02 +/- 0.08). Unilateral and bilateral carotid baroreflex stimulation abolished the right prevalence of A(N) and AA(N). In conclusion, the right lateralization of sympathetic activity to the vessels is indicated by normalized burst strength parameters of bilateral MSNA recordings at rest during spontaneous breathing. Carotid baroreceptor stimulation disrupted such expression of MSNA lateralization possibly by disturbing the synchronizing action of right cerebral hemisphere.

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Year:  2009        PMID: 19363133      PMCID: PMC2716107          DOI: 10.1152/ajpheart.01045.2008

Source DB:  PubMed          Journal:  Am J Physiol Heart Circ Physiol        ISSN: 0363-6135            Impact factor:   4.733


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