The accurate measurement of sympathetic nerve activity is essential for advancing knowledge related to the mechanisms that underpin sympathetic activation in diseased states, such as acute heart failure. Considering sympathetic outflow throughout the body is differentially modulated, the most reliable method of measuring sympathetic traffic to individual organs is by way of direct electrophysiological recording of nerve activity. However, the surgical approach of accessing, exposing, and isolating the sympathetic nerve of interest is technically demanding, especially in the small size of a standard laboratory rat, one of the most common models for measuring SNA. Moreover, preserving the health of the nerve while attaching it to electrodes for recording requires careful diligence. The complexity of recording from specifically the cardiac sympathetic nerve remains a significant challenge due to the difficulty of accessing the nerve within the thorax cavity. Here, we describe in detail the process of surgically isolating the cardiac sympathetic nerve activity in a rat for accurately recording and quantifying sympathetic nerve activity.
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http://dx.doi.org/10.1007/978-1-0716-4342-6_15 | DOI Listing |
Cereb Cortex
December 2024
Baker Department of Cardiometabolic Health, The University of Melbourne, Grattan Street, Parkville, VIC 3010, Australia.
Transcranial magnetic stimulation (TMS) is applied both in research settings and clinically, notably in treating depression through the dorsolateral prefrontal cortex (dlPFC). We have recently shown that transcranial alternating current stimulation of the dlPFC partially entrains muscle sympathetic nerve activity (MSNA) to the stimulus. We, therefore, aimed to further explore the sympathetic properties of the dlPFC, hypothesizing that single-pulse TMS could generate de novo MSNA bursts.
View Article and Find Full Text PDFJACC Clin Electrophysiol
November 2024
Electrophysiology Section, Division of Cardiology, Hunter Holmes McGuire VA Medical Center, Richmond, Virginia, USA; Pauley Heart Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA. Electronic address:
Background: The mechanisms underlying postoperative atrial fibrillation (POAF) remain unclear.
Objectives: The aim of this study was to test the hypothesis that targeted chemical ganglionated plexi (GP) modulation of all major left atrial-pulmonary vein GP using novel nanoformulated calcium chloride (nCaCl) can reverse postoperative neuroelectrical remodeling by suppressing vagosympathetic nerve activity and the localized inflammatory process, both critical substrates of POAF.
Methods: In a novel canine model of POAF with serial thoracopericardiotomies, sympathetic nerve activity (SNA), vagal nerve activity (VNA) and GP nerve activity (GPNA) were recorded; spontaneous and in vivo AF vulnerability were assessed; and atrial and circulating inflammatory markers and norepinephrine (NE) were measured to determine the neuroelectrical remodeling that promotes POAF and its subsequent modulation with nCaCl GP treatment (n = 6) vs saline sham controls (n = 6).
Am J Physiol Regul Integr Comp Physiol
December 2024
Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Japan.
The assessment of adrenergic modulation of sweating as assessed via pharmacologic administration of α- and β-adrenergic receptor blockers during exercise has yielded mixed findings. However, the underlying mechanisms for this disparity remains unresolved. We investigated the effects of separate and combined blockade of α- and β-adrenergic receptors on forearm sweating induced by a 30-min moderate-intensity exercise bout (n=17, protocol 1) and the administration of adrenergic agonists epinephrine and norepinephrine (n=16, protocol 2) in the heat.
View Article and Find Full Text PDFJ Neurophysiol
December 2024
Dalton Cardiovascular Research Center, University of Missouri, 1500 Research Park Drive, Columbia, Missouri, 65211, USA.
Methods Mol Biol
December 2024
Department of Physiology, School of Biomedical Science, University of Otago, Dunedin, New Zealand.
The accurate measurement of sympathetic nerve activity is essential for advancing knowledge related to the mechanisms that underpin sympathetic activation in diseased states, such as acute heart failure. Considering sympathetic outflow throughout the body is differentially modulated, the most reliable method of measuring sympathetic traffic to individual organs is by way of direct electrophysiological recording of nerve activity. However, the surgical approach of accessing, exposing, and isolating the sympathetic nerve of interest is technically demanding, especially in the small size of a standard laboratory rat, one of the most common models for measuring SNA.
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