Bilateral Carotid Sinus Nerve Electrical Stimulation (Baropacer) Therapy of Refractory Hypertension.

1972 ◽  
Vol 76 (5) ◽  
pp. 875
Author(s):  
Allan B. Schwartz
Keyword(s):  
Electrical Stimulation ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Refractory Hypertension ◽  
Bilateral Carotid

Central and peripheral chemoreceptor inputs to phrenic and hypoglossal motoneurons

1982 ◽  
Vol 53 (6) ◽  
pp. 1504-1511 ◽  
Author(s):  
E. N. Bruce ◽  
J. Mitra ◽  
N. S. Cherniack
Keyword(s):  
Opposite Effect ◽  
Carotid Sinus ◽  
Ventral Surface ◽  
Carotid Sinus Nerve ◽  
Peripheral Chemoreceptor ◽  
Hypoglossal Motoneurons ◽  
Nerve Response ◽  
Bilateral Carotid ◽  
Hypoglossal Motoneuron ◽  
Before And After

We tested the hypothesis that phrenic and hypoglossal responses to progressive hypercapnia differ qualitatively because the CO2-related drive inputs to their respective motoneuron pools are different. The relative contributions of carotid sinus and central chemoreceptor inputs to hypoglossal and phrenic responses during hyperoxic hypercapnia were determined by comparing the two nerve activities during rebreathing runs done either before and after bilateral carotid sinus nerve (CSN) section, or without and with cooling of the intermediate, I(s), area on the ventral surface of the medulla. The studies were performed on chloralose-anesthetized, vagotomized, paralyzed cats. Cooling of the I(s) area impaired phrenic responsiveness to hypercapnia more than hypoglossal responsiveness, whereas CSN section had the opposite effect. Thus phrenic nerve response was more dependent on central chemoreceptor input than was the hypoglossal response, but hypoglossal response was more dependent on carotid sinus chemoreceptor input. We conclude that the phrenic and hypoglossal motoneuron pools each receive a different functional input from both the medullary and the carotid sinus chemoreceptors.

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku
Keyword(s):  
Electrical Stimulation ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Chemical Stimulation ◽  
Respiratory Drive ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Respiratory Reflexes ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

scholarly journals Carotid sinus nerve stimulation attenuates alveolar bone loss and inflammation in experimental periodontitis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Aline Barbosa Ribeiro ◽  
Fernanda Brognara ◽  
Josiane Fernandes da Silva ◽  
Jaci Airton Castania ◽  
Patrícia Garani Fernandes ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Carotid Sinus ◽  
Inflammatory Responses ◽  
Periodontal Diseases ◽  
Alveolar Bone Loss ◽  
Carotid Sinus Nerve ◽  
Mandibular Molar ◽  
Inflammatory Processes

Abstract Baroreceptor and chemoreceptor reflexes modulate inflammatory responses. However, whether these reflexes attenuate periodontal diseases has been poorly examined. Thus, the present study determined the effects of electrical activation of the carotid sinus nerve (CSN) in rats with periodontitis. We hypothesized that activation of the baro and chemoreflexes attenuates alveolar bone loss and the associated inflammatory processes. Electrodes were implanted around the CSN, and bilateral ligation of the first mandibular molar was performed to, respectively, stimulate the CNS and induce periodontitis. The CSN was stimulated daily for 10 min, during nine days, in unanesthetized animals. On the eighth day, a catheter was inserted into the left femoral artery and, in the next day, the arterial pressure was recorded. Effectiveness of the CNS electrical stimulation was confirmed by hypotensive responses, which was followed by the collection of a blood sample, gingival tissue, and jaw. Long-term (9 days) electrical stimulation of the CSN attenuated bone loss and the histological damage around the first molar. In addition, the CSN stimulation also reduced the gingival and plasma pro-inflammatory cytokines induced by periodontitis. Thus, CSN stimulation has a protective effect on the development of periodontal disease mitigating alveolar bone loss and inflammatory processes.

scholarly journals Carotid sinus nerve electrical stimulation in conscious rats attenuates systemic inflammation via chemoreceptor activation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Fernanda Machado Santos-Almeida ◽  
Gean Domingos-Souza ◽  
César A. Meschiari ◽  
Laura Campos Fávaro ◽  
Christiane Becari ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Systemic Inflammation ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Conscious Rats

scholarly journals Electrostimulation of the carotid sinus nerve in mice attenuates inflammation via glucocorticoid receptor on myeloid immune cells

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Aidan Falvey ◽  
Fabrice Duprat ◽  
Thomas Simon ◽  
Sandrine Hugues-Ascery ◽  
Silvia V. Conde ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Glucocorticoid Receptor ◽  
Tumour Necrosis Factor ◽  
Immune Cells ◽  
Tumour Necrosis ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Tumour Necrosis Factor Production ◽  
Anti Inflammatory ◽  
Necrosis Factor

Abstract Background The carotid bodies and baroreceptors are sensors capable of detecting various physiological parameters that signal to the brain via the afferent carotid sinus nerve for physiological adjustment by efferent pathways. Because receptors for inflammatory mediators are expressed by these sensors, we and others have hypothesised they could detect changes in pro-inflammatory cytokine blood levels and eventually trigger an anti-inflammatory reflex. Methods To test this hypothesis, we surgically isolated the carotid sinus nerve and implanted an electrode, which could deliver an electrical stimulation package prior and following a lipopolysaccharide injection. Subsequently, 90 min later, blood was extracted, and cytokine levels were analysed. Results Here, we found that carotid sinus nerve electrical stimulation inhibited lipopolysaccharide-induced tumour necrosis factor production in both anaesthetised and non-anaesthetised conscious mice. The anti-inflammatory effect of carotid sinus nerve electrical stimulation was so potent that it protected conscious mice from endotoxaemic shock-induced death. In contrast to the mechanisms underlying the well-described vagal anti-inflammatory reflex, this phenomenon does not depend on signalling through the autonomic nervous system. Rather, the inhibition of lipopolysaccharide-induced tumour necrosis factor production by carotid sinus nerve electrical stimulation is abolished by surgical removal of the adrenal glands, by treatment with the glucocorticoid receptor antagonist mifepristone or by genetic inactivation of the glucocorticoid gene in myeloid cells. Further, carotid sinus nerve electrical stimulation increases the spontaneous discharge activity of the hypothalamic paraventricular nucleus leading to enhanced production of corticosterone. Conclusion Carotid sinus nerve electrostimulation attenuates inflammation and protects against lipopolysaccharide-induced endotoxaemic shock via increased corticosterone acting on the glucocorticoid receptor of myeloid immune cells. These results provide a rationale for the use of carotid sinus nerve electrostimulation as a therapeutic approach for immune-mediated inflammatory diseases.

Abstract 032: Carotid Chemoreceptor Activation Blunts The Hypotensive Response Caused By The Electrical Stimulation Of The Carotid Sinus In Conscious Rats

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Pedro L Katayama ◽  
Jaci A Castania ◽  
Rubens Fazan ◽  
Helio C Salgado
Keyword(s):  
Electrical Stimulation ◽  
Resistant Hypertension ◽  
Carotid Sinus ◽  
Hemodynamic Responses ◽  
Carotid Chemoreceptors ◽  
Conscious Rats ◽  
Carotid Baroreceptors ◽  
Bilateral Carotid ◽  
Hypotensive Response ◽  
Stimulation Of

The mechanisms involved in Baroreflex Activation Therapy (BAT) in patients with resistant hypertension require better understanding. It was shown that electrical stimulation of the carotid sinus (ESCS), in conscious carotid body-denervated rats, caused bradycardia and greater hypotensive response when compared with intact control rats. In the current study the activation of the chemoreceptors due to ESCS, in conscious rats, was examined in the absence of the carotid baroreceptors. Wistar rats with unilateral denervation of the right carotid chemoreceptors were divided into three groups: 1) control (CONT, n=7); 2) bilateral carotid chemoreceptor denervation (CD, n=7); 3) unilateral denervation of the left carotid baroreceptors (BD, n=4). Under ketamine/xylazine anesthesia bipolar electrodes were implanted around the left carotid sinus combined with arterial and venous catheters into the femoral vessels. On the next day, after basal hemodynamic recordings, the animals received three ESCS (5V, 1 ms) with 15 Hz, 30 Hz and 60 Hz, applied randomly for 20s. Carotid chemoreceptors denervation was confirmed by the lack of hemodynamic responses after the administration of KCN (40 μg iv). The efficacy of left carotid baroreceptor denervation was confirmed by the absence of hemodynamic responses to changes in the left carotid sinus pressure ranging from 60 mmHg to 180 mmHg. The results showed that ESCS was efficient to cause greater hypotensive responses in the CD as compared with the CONT group at 60 Hz (-37 ± 6 vs -19 ± 3 mmHg) and to cause hypertensive responses in the BD group at 30 Hz and 60 Hz (15 ± 2 and 19 ± 2 mmHg). ESCS caused no alteration of the heart rate in the CONT but caused significant bradycardia in the CD group at 30 Hz and 60 Hz (-31 ± 11 and -35 ± 12 bpm) and in the BD group at 15 Hz, 30 Hz and 60 Hz (-38 ± 6, -37 ± 6 and -34 ± 4 bpm). These data demonstrated that carotid chemoreceptor activation in the absence of the carotid baroreceptors caused hypertension and bradycardia, indicating that when the baroreceptors are intact, the chemoreceptors blunt the hypotensive response caused by ESCS. These findings provide important information for the clinical studies using BAT in patients with resistant hypertension and/or heart failure.

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