LATE PERSONAL RESULTS IN THE TREATMENT OF ERB-GOLDFLAM MYASTHENIA IN 30 CASES BY BILATERAL CAROTID SINUS DENERVATION

1959 ◽  
pp. 373-375
Author(s):  
L. STEPIEŃ
Keyword(s):  
Carotid Sinus ◽  
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.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Summation of dynamic transfer characteristics of left and right carotid sinus baroreflexes in rabbits

1999 ◽  
Vol 277 (3) ◽  
pp. H857-H865 ◽  
Author(s):  
Toru Kawada ◽  
Takayuki Sato ◽  
Toshiaki Shishido ◽  
Masashi Inagaki ◽  
Teiji Tatewaki ◽  
...  
Keyword(s):  
Transfer Function ◽  
Transfer Functions ◽  
Carotid Sinus ◽  
Aortic Pressure ◽  
Operating Pressure ◽  
Dynamic Interactions ◽  
Transfer Characteristics ◽  
Bilateral Carotid ◽  
Steady State Responses ◽  
State Responses

Although interactions among parallel negative-feedback baroreflex systems have been extensively investigated with respect to their steady-state responses, the dynamic interactions remain unknown. In anesthetized, vagotomized, and aortic-denervated rabbits, we perturbed isolated intracarotid sinus pressure (CSP) unilaterally or bilaterally around the physiological operating pressure according to binary white noise. The neural arc transfer function from CSP to cardiac sympathetic nerve activity (SNA) and the peripheral arc transfer function from SNA to aortic pressure were estimated. The gain values of the neural arc at 0.01 Hz estimated by the left (L) and right (R) CSP perturbations were 0.94 ± 0.31 and 0.96 ± 0.25, respectively. The gain value increased to 2.17 ± 0.97 during the bilateral identical CSP perturbation and was not significantly different from L + R. The phase values of the neural arc did not differ among protocols. No significant differences were observed in the peripheral arc transfer functions among protocols. We conclude that summation of the dynamic transfer characteristics of the bilateral carotid sinus baroreflexes around the physiological operating pressure approximates simple addition.

Reflex limb dilatation following norepinephrine and angiotensin II in conscious dogs

1976 ◽  
Vol 230 (3) ◽  
pp. 557-563 ◽  
Author(s):  
SF Vatner ◽  
RJ McRitchie
Keyword(s):  
Angiotensin Ii ◽  
Iliac Artery ◽  
Carotid Sinus ◽  
Conscious Dogs ◽  
Beta Blockade ◽  
Prostaglandin Synthetase ◽  
Nerve Section ◽  
Iliac Arteries ◽  
Bilateral Carotid ◽  
Bilateral Vagotomy

Effects of intravenous and intra-arterial norepinephrine (NE) and angiotensin II (AN) were compared in 18 conscious dogs instrumented with Doppler or electromagnetic flow probes on the iliac, mesenteric, and renal arteries, and catheters in the aorta and iliac arteries. NE and AN administered intravenously constricted the mesenteric and renal beds, and constricted the iliac bed when administered directly into the iliac artery. In contrast, intravenous NE and AN caused striking reflex increases in iliac flow and reductions in iliac resistance, respectively, in 12 of 18 dogs studied. The reflex iliac dilatation was not prevented by beta blockade with propranolol, cholinergic blockade with atropine, or prostaglandin synthetase inhibition with indomethacin. However, the responses were abolished by either phentolamine, 1 mg/kv iv, or after local blockade of the limb with either phentolamine, 0.5 mg/kg, or with tripelennamine, 2 mg/kg. The dilatation was not prevented by either bilateral carotid sinus and aortic nerve section or by bilateral vagotomy alone, but was prevented by a combination of these procedures. Thus, intravenous NE and AN cause striking reflex iliac dilatation in the limb in the conscious dog; the afferent arc of this reflex involves both arterial baroreceptor and vagal pathways, while the efferent mechanism involves an interaction of alpha-adrenergic and histaminergic receptors.

Baroreceptor and chemoreceptor contributions to the hypertensive response to bilateral carotid occlusion in conscious mice

2010 ◽  
Vol 299 (6) ◽  
pp. H1990-H1995 ◽  
Author(s):  
R. M. Lataro ◽  
J. A. Castania ◽  
M. W. Chapleau ◽  
H. C. Salgado ◽  
R. Fazan
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Peripheral Chemoreceptor ◽  
Femoral Catheter ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
C57bl Mice ◽  
Common Carotid Arteries ◽  
Sustained Increase

This study aimed to characterize the role played by baroreceptors and chemoreceptors in the hypertensive response to bilateral carotid occlusion (BCO) in conscious C57BL mice. On the day before the experiments the animals were implanted with pneumatic cuffs around their common carotid arteries and a femoral catheter for measurement of arterial pressure. Under the same surgical approach, groups of mice were submitted to aortic or carotid sinus denervation or sham surgery. BCO was performed for 30 or 60 s, promoting prompt and sustained increase in mean arterial pressure and fall in heart rate. Compared with intact mice, the hypertensive response to 30 s of BCO was enhanced in aortic-denervated mice (52 ± 4 vs. 41 ± 4 mmHg; P < 0.05) but attenuated in carotid sinus-denervated mice (15 ± 3 vs. 41 ± 4 mmHg; P < 0.05). Suppression of peripheral chemoreceptor activity by hyperoxia [arterial partial pressure of oxygen (PaO2) > 500 mmHg] attenuated the hypertensive response to BCO in intact mice (30 ± 6 vs. 51 ± 5 mmHg in normoxia; P < 0.05) and abolished the bradycardia. It did not affect the hypertensive response in carotid sinus-denervated mice (20 ± 4 vs. 18 ± 3 mmHg in normoxia; P < 0.05). The attenuation of the hypertensive response to BCO by carotid sinus denervation or hyperoxia indicates that the hypertensive response in conscious mice is mediated by both baro- and chemoreceptors. In addition, aortic denervation potentiates the hypertensive response elicited by BCO in conscious mice.

Role of peripheral and central chemoreceptors in the initiation of fetal respiration

1975 ◽  
Vol 38 (3) ◽  
pp. 407-410 ◽  
Author(s):  
V. Chernick ◽  
E. E. Faridy ◽  
R. D. Pagtakhan
Keyword(s):  
Carotid Sinus ◽  
Blood Gases ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Central Chemoreceptors ◽  
Bilateral Carotid ◽  
Fetal Respiration ◽  
A Minor ◽  
The Relationship

The relationship between fetal femoral arterial P02 and PC02 was evalulated in 13 fetal sheep with intact and denervated peripheral chemoreceptors. With intact chemoreceptors, a significant relationship was found between fetal Pa02 and PaC02 at the time of the first breath (Pa02 = 2.57 + 0.09 PaC02; r = 0.62, P less than 0.05)mfollowing bilateral carotid sinus nerve section (CSN) or total peripheral chemodenervation (TD), PaC02. Comparison of the intact, CSN, and TD blood gases at the time of the first breath demonstrated that a) severe hypoxemia stimulates fetal respiration even following total peripheral chemodenervation; b) fetal central chemoreceptors do not respond to PaC02; c) PaC02 acting via peripheral chemoreceptors has a minor modulating effect on the degree of hypoxemia required to initiate fetal respiration. At a PaC02 below 40 mmHg this effect is inhibitory, acting via the carotid body. At a PaC02 above 90 mmHg this effect is stimulatory, acting via both carotid and aortic bodies.

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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