The Effect of Sympathetic Nerve Stimulation on Ventilation and Upper Airway Resistance in the Anaesthetized Rat

O’Halloran, K. D.; Curran, A. K.; Bradford, Aidan

doi:10.1007/978-1-4615-5891-0_68

Cited by 4 publications

(3 citation statements)

References 6 publications

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“…The projections of the SCG to a series of inter-related structures, such as the carotid body and carotid sinus, upper airway and tongue (Flett and Bell, 1991;Kummer et al, 1992;O'Halloran et al, 1996O'Halloran et al, , 1998Hisa et al, 1999;Wang and Chiou, 2004;Oh et al, 2006), and nuclei within the hypothalamus and brainstem, including the nucleus tractus solitarius (nTS) (Cardinali et al, 1981a(Cardinali et al, ,b, 1982Gallardo et al, 1984;Saavedra, 1985;Wiberg and Widenfalk, 1993;Westerhaus and Loewy, 1999;Esquifino et al, 2004;Hughes-Davis et al, 2005;Mathew, 2007), provide evidence that the SCG is a vital integrative structure regulating cardiorespiratory function. Previous studies have shown that electrical stimulation of the CSC decreases arterial blood pressure and upper airway resistance in rats (O'Halloran et al, 1996(O'Halloran et al, , 1998. Moreover, there is substantial (and conflicting) evidence as to the ability of sympathetic innervation to the carotid body to influence resting activity of glomus cells and chemoafferents within the carotid sinus nerve (CSN), and modulate changes in activity during hypoxic gas challenge (HXC) (Prabhakar, 1994).…”

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confidence: 99%

Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

et al. 2021

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The cervical sympathetic chain (CSC) innervates post-ganglionic sympathetic neurons within the ipsilateral superior cervical ganglion (SCG) of all mammalian species studied to date. The post-ganglionic neurons within the SCG project to a wide variety of structures, including the brain (parenchyma and cerebral arteries), upper airway (e.g., nasopharynx and tongue) and submandibular glands. The SCG also sends post-ganglionic fibers to the carotid body (e.g., chemosensitive glomus cells and microcirculation), however, the function of these connections are not established in the mouse. In addition, nothing is known about the functional importance of the CSC-SCG complex (including input to the carotid body) in the mouse. The objective of this study was to determine the effects of bilateral transection of the CSC on the ventilatory responses [e.g., increases in frequency of breathing (Freq), tidal volume (TV) and minute ventilation (MV)] that occur during and following exposure to a hypoxic gas challenge (10% O2 and 90% N2) in freely-moving sham-operated (SHAM) adult male C57BL6 mice, and in mice in which both CSC were transected (CSCX). Resting ventilatory parameters (19 directly recorded or calculated parameters) were similar in the SHAM and CSCX mice. There were numerous important differences in the responses of CSCX and SHAM mice to the hypoxic challenge. For example, the increases in Freq (and associated decreases in inspiratory and expiratory times, end expiratory pause, and relaxation time), and the increases in MV, expiratory drive, and expiratory flow at 50% exhaled TV (EF50) occurred more quickly in the CSCX mice than in the SHAM mice, although the overall responses were similar in both groups. Moreover, the initial and total increases in peak inspiratory flow were higher in the CSCX mice. Additionally, the overall increases in TV during the latter half of the hypoxic challenge were greater in the CSCX mice. The ventilatory responses that occurred upon return to room-air were essentially similar in the SHAM and CSCX mice. Overall, this novel data suggest that the CSC may normally provide inhibitory input to peripheral (e.g., carotid bodies) and central (e.g., brainstem) structures that are involved in the ventilatory responses to hypoxic gas challenge in C57BL6 mice.

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Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

et al. 2021

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“…SCG is located at the cervical sympathetic chain, which contains post-ganglionic sympathetic fibers ( Tang et al, 1995a ; Tang et al, 1995b ; Tang et al, 1995c ; Llewellyn-Smith et al, 1998 ). Multiple studies provide evidence that post-ganglionic fibrers from the SCG innervate a series of inter-related structures including the carotid body and carotid sinus, tongue and upper airway ( Flett and Bell, 1991 ; O’Halloran et al, 1996 ; Wang et al, 2018 ), and brainstem nuclei, such as the NTS ( Gallardo et al, 1984 ; Hughes-Davis et al, 2005 ). Felippe et al (2022) , provided evidence that SCG mediated CB hyperexcitability and sensitized the chemoreflex in spontaneously hypertensive (SH) rats.…”

Section: Discussionmentioning

confidence: 99%

The superior cervical ganglion is involved in chronic chemoreflex sensitization during recovery from acute lung injury

Kamra

Karpuk²,

Zucker³

et al. 2023

Front. Physiol.

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Introduction: Acute lung injury (ALI) initiates an inflammatory cascade that impairs gas exchange, induces hypoxemia, and causes an increase in respiratory rate (fR). This stimulates the carotid body (CB) chemoreflex, a fundamental protective reflex that maintains oxygen homeostasis. Our previous study indicated that the chemoreflex is sensitized during the recovery from ALI. The superior cervical ganglion (SCG) is known to innervate the CB, and its electrical stimulation has been shown to significantly sensitize the chemoreflex in hypertensive and normotensive rats. We hypothesized that the SCG is involved in the chemoreflex sensitization post-ALI.Methods: We performed a bilateral SCG ganglionectomy (SCGx) or sham-SCGx (Sx) in male Sprague Dawley rats 2 weeks before inducing ALI (Week −2 i.e., W-2). ALI was induced using a single intra-tracheal instillation of bleomycin (bleo) (day 1). Resting-fR, Vt (Tidal Volume), and V̇ E (Minute Ventilation) were measured. The chemoreflex response to hypoxia (10% O2, 0% CO2) and normoxic-hypercapnia (21% O2, 5% CO2) were measured before surgery on W (−3), before bleo administration on W0 and on W4 post-bleo using whole-body plethysmography (WBP).Results: SCGx did not affect resting fR, Vt and V̇E as well as the chemoreflex responses to hypoxia and normoxic hypercapnia in either group prior to bleo. There was no significant difference in ALI-induced increase in resting fR between Sx and SCGx rats at W1 post-bleo. At W4 post-bleo, there were no significant differences in resting fR, Vt, and V̇E between Sx and SCGx rats. Consistent with our previous study, we observed a sensitized chemoreflex (delta fR) in response to hypoxia and normoxic hypercapnia in Sx rats at W4 post-bleo. However, at the same time, compared to Sx rats, the chemoreflex sensitivity was significantly less in SCGx rats in response to either hypoxia or normoxic hypercapnia.Discussion: These data suggest that SCG is involved in the chemoreflex sensitization during ALI recovery. Further understanding of the underlying mechanism will provide important information for the long-term goal of developing novel targeted therapeutic approaches to pulmonary diseases to improve clinical outcomes.

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“…While providing evidence that the CSC-SCG complex has a role in modulating the hypoxic ventilatory response (HVR), the exact pathways and target structures by which this complex regulates the HVR were not elucidated in these mouse studies. It is well-known that, post-ganglionic nerves in the SCG project to target structures in the head and neck via the external (ECN) and the internal (ICN) carotid nerves ( Bowers and Zigmond, 1979 ; Buller and Bolter, 1997 ; Asamoto, 2004 ; Savastano et al, 2010 ) including, the upper airway and tongue ( Flett and Bell, 1991 ; Kummer et al, 1992 ; O'Halloran et al, 1996 ; O'Halloran et al, 1998 ; Hisa et al, 1999 ; Wang and Chiou, 2004 ; Oh et al, 2006 ), vascular structures within the brain including the Circle of Willis and cerebral arteries ( Sadoshima et al, 1981 ; Sadoshima et al, 1983a ; Sadoshima et al, 1983b ; Werber and Heistad, 1984 ), and nuclei in the hypothalamus and brainstem ( Cardinali et al, 1981a ; Cardinali et al, 1981b ; Cardinali et al, 1982 ; Gallardo et al, 1984 ; Saavedra, 1985 ; Wiberg and Widenfalk, 1993 ; Westerhaus and Loewy, 1999 ; Esquifino et al, 2004 ; Hughes-Davis et al, 2005 ; Mathew, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

Loss of ganglioglomerular nerve input to the carotid body impacts the hypoxic ventilatory response in freely-moving rats

2023

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The carotid bodies are the primary sensors of blood pH, pO2 and pCO2. The ganglioglomerular nerve (GGN) provides post-ganglionic sympathetic nerve input to the carotid bodies, however the physiological relevance of this innervation is still unclear. The main objective of this study was to determine how the absence of the GGN influences the hypoxic ventilatory response in juvenile rats. As such, we determined the ventilatory responses that occur during and following five successive episodes of hypoxic gas challenge (HXC, 10% O2, 90% N2), each separated by 15 min of room-air, in juvenile (P25) sham-operated (SHAM) male Sprague Dawley rats and in those with bilateral transection of the ganglioglomerular nerves (GGNX). The key findings were that 1) resting ventilatory parameters were similar in SHAM and GGNX rats, 2) the initial changes in frequency of breathing, tidal volume, minute ventilation, inspiratory time, peak inspiratory and expiratory flows, and inspiratory and expiratory drives were markedly different in GGNX rats, 3) the initial changes in expiratory time, relaxation time, end inspiratory or expiratory pauses, apneic pause and non-eupneic breathing index (NEBI) were similar in SHAM and GGNX rats, 4) the plateau phases obtained during each HXC were similar in SHAM and GGNX rats, and 5) the ventilatory responses that occurred upon return to room-air were similar in SHAM and GGNX rats. Overall, these changes in ventilation during and following HXC in GGNX rats raises the possibility the loss of GGN input to the carotid bodies effects how primary glomus cells respond to hypoxia and the return to room-air.

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The Effect of Sympathetic Nerve Stimulation on Ventilation and Upper Airway Resistance in the Anaesthetized Rat

Cited by 4 publications

References 6 publications

Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

The superior cervical ganglion is involved in chronic chemoreflex sensitization during recovery from acute lung injury

Loss of ganglioglomerular nerve input to the carotid body impacts the hypoxic ventilatory response in freely-moving rats

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