scholarly journals Restoration of hypoxic respiratory responses in the awake rat after carotid body denervation by sinus nerve section.

1986 ◽  
Vol 380 (1) ◽  
pp. 61-73 ◽  
Author(s):  
R L Martin-Body ◽  
G J Robson ◽  
J D Sinclair
Keyword(s):  
Carotid Body ◽  
Nerve Section ◽  
Awake Rat ◽  
Respiratory Responses ◽  
Carotid Body Denervation

Plasticity of cardiovascular chemoreflexes after prolonged unilateral carotid body denervation: implications for its therapeutic use

2020 ◽  
Vol 318 (5) ◽  
pp. H1325-H1336
Author(s):  
Jaime Eugenín ◽  
Carolina Larraín ◽  
Patricio Zapata
Keyword(s):  
Carotid Body ◽  
Therapeutic Use ◽  
Therapeutic Effectiveness ◽  
Sympathetic Outflow ◽  
Sympathetic Hyperactivity ◽  
Functional Changes ◽  
Human Disorders ◽  
Carotid Body Denervation

Unilateral carotid body denervation has been proposed as treatment for sympathetic hyperactivity-related human disorders. Its therapeutic effectiveness for maintaining a persistent decrease in the sympathetic outflow activity will depend on the absence of compensatory chemoreflex plasticity in the remnant carotid and aortic afferents. Here, we suggest that the integrity of central afferents after carotid body denervation is essential to prevent the emergence of plastic functional changes on the contralateral “intact” carotid nerve.

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 Body Denervation Markedly Improves Survival in Rats With Hypertensive Heart Failure

2017 ◽  
Vol 30 (8) ◽  
pp. 791-798 ◽  
Author(s):  
Kana Fujii ◽  
Keita Saku ◽  
Takuya Kishi ◽  
Yasuhiro Oga ◽  
Takeshi Tohyama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Carotid Body ◽  
Carotid Body Denervation

Effect of carotid body denervation on arousal response to hypoxia in sleeping dogs

1981 ◽  
Vol 51 (1) ◽  
pp. 40-45 ◽  
Author(s):  
G. Bowes ◽  
E. R. Townsend ◽  
L. F. Kozar ◽  
S. M. Bromley ◽  
E. A. Phillipson
Keyword(s):  
Carotid Body ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Critical Role ◽  
Ventilatory Responses ◽  
Progressive Hypoxia ◽  
Arousal Response ◽  
Arterial O2 Saturation ◽  
Carotid Body Denervation

We studied the arousal and ventilatory responses to hypoxia during sleep in three trained dogs, before and 1–4 wk after carotid body denervation (CBD). During the studies the dogs breathed through a cuffed endotracheal tube inserted via a chronic tracheostomy. Eucapnic progressive hypoxia was induced by a rebreathing technique, and arterial O2 saturation (Sao2) was measured with an ear oximeter. Sleep stage was determined by electroencephalographic and behavioral criteria. Following CBD, all dogs exhibited hypoventilation under resting conditions; hypoxic ventilatory responses during wakefulness, slow-wave sleep (SWS), and rapid-eye-movement (REM) sleep were less than 10% of control. Prior to CBD, hypoxic arousal occurred at Sao2 of 83.2 +/- 4.6% (mean +/- Se) during SWS and 70.6 +/-2.2% in REM sleep. Following CBD, arousal failed to occur during progressive desaturation to 60% in SWS and 50% in REM sleep, at which levels hypoxia was arbitrarily terminated. In a few studies following CBD where rebreathing was allowed to continue, the dogs occasionally failed to arouse at all and require active resuscitation. The results indicate a critical role for the carotid chemoreceptors in mediating the arousal response to hypoxia.

scholarly journals Carotid body denervation does not affect CO2 sensitivity in multiple rat strains

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Gary Charles Mouradian ◽  
Justin Miller ◽  
Clarissa Muere ◽  
Hubert V. Forster ◽  
Matthew R. Hodges
Keyword(s):  
Carotid Body ◽  
Rat Strains ◽  
Co2 Sensitivity ◽  
Carotid Body Denervation

Abstract 17082: Carotid Body Denervation Improves Autonomic Balance and Prevents the Worsening of Heart Failure in Rats After Large Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Keita Saku ◽  
Takuya Kishi ◽  
Akiko Nishizaki ◽  
Kana Fujii ◽  
Takuya Akashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Carotid Body ◽  
High Frequency ◽  
Diastolic Pressure ◽  
Plasma Norepinephrine ◽  
Autonomic Balance ◽  
Sprague Dawley ◽  
Lung Weight ◽  
Carotid Body Denervation

Introduction: Carotid body denervation (CBD) abolishes the carotid body hypersensitivity induced sympathoexcitatory hypertension. Since the carotid body hypersensitivity is a salient feature and predicts poor outcome of chronic heart failure (CHF), we hypothesized that CBD restores normal autonomic balance, thus improves CHF in rats after large myocardial infarction (MI). Methods: We created MI in 8 weeks Sprague-Dawley rats. Surviving rats at 2 weeks after MI were randomized into CBD (n=11) and sham-operated (Sham; n=13) groups. We removed the tissues around the carotid bifurcation and established CBD. In some rats (Sham; n=5, CBD; n=5), we telemetrically recorded heart rate (HR). One month after CBD, we compared physiological, histological and immunochemical findings between CBD and Sham. Results: CBD significantly reduced HR (337±15 vs. 364±12 bpm, p<0.05). CBD markedly increased the power spectral density of HR in the high frequency range (81.0±9.5 vs. 29.0±8.2 n.u., p<0.05) and decreased that of the low frequency/high frequency ratio (0.6±0.2 vs. 1.8±0.5, p<0.05) indicating the restoration of autonomic balance. CBD significantly reduced biventricular weight (3.1±0.3 vs. 3.7±0.3 g/kg, p<0.05) and left ventricle (LV) end-diastolic pressure (22±5 vs. 33±5 mmHg, p<0.01) and increased maximum LV dp/dt (5118±809 vs. 4217±472 mmHg/sec, p<0.05). CBD reduced lung weight (a marker of pulmonary edema) (6.8±2.0 vs. 12.4±1.5 g/kg, p<001). Furthermore, CBD reduced plasma brain natriuretic peptide (70±43 vs. 166±71 pg/ml, p<0.01) and plasma norepinephrine as an index of sympathetic drive (384±202 vs. 1048±997 pg/ml, p<0.05). CBD significantly reduced the number of inflammatory macrophages (345±45 vs. 474±73 counts/mm2, p<0.05) in the LV and the plasma concentration of interleukin-1β (14.3±4.7 vs. 24.5±11.8 pg/ml, p<0.05) indicating that CBD also suppressed the inflammatory response in CHF. Conclusions: CBD restores normal autonomic balance and prevents the worsening of heart failure in rats after large myocardial infarction. CBD may serve as a novel neuro-modulatory therapy for CHF patients.

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