Reversible vascular isolation of carotid sinuses in conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H809-H814 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Response Curves ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Before And After ◽  
Surgical Preparation ◽  
Sinus Pressure

A surgical technique has been developed that permits reversible vascular isolation of both carotid sinuses in the conscious dog. Seven dogs so prepared were studied over periods of 4-12 wk. Repeatable stimulus-response curves relating arterial blood pressure to carotid sinus pressure were obtained for sinus pressures of 40-240 mmHg. Two studies gave evidence that the ability of the carotid baroreceptors to influence arterial pressure was not or was minimally affected by the surgical dissection. In 10 dogs one sinus was surgically prepared; 3 wk later the dogs were anesthetized and vagotomized. The steady-state stimulus-response curves for the chronically prepared sinuses showed no consistent differences from the curves for the opposite, acutely prepared sinuses. In 8 other dogs the hypertensive responses to bilateral carotid occlusion were compared before and after surgical preparation of both sinuses. The responses to carotid occlusion tended to be decreased after surgery but the differences were small and were significant only in 3 dogs.

Constriction of lymphatics by catecholamines, carotid occlusion, or hemorrhage

1988 ◽  
Vol 255 (3) ◽  
pp. H514-H524
Author(s):  
J. M. Dabney ◽  
M. J. Buehn ◽  
D. E. Dobbins
Keyword(s):  
Lymphatic Vessel ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Carotid Occlusion ◽  
Central Venous ◽  
Lymphatic Function ◽  
Hemorrhagic Hypotension ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

Regulation of lymphatics by sympathetic nerves or hormones seems probable. To elucidate this, we perfused a lymphatic vessel in the paw of the anesthetized dog while measuring lymphatic perfusion pressure. We studied the effects of norepinephrine, epinephrine, hemorrhage, and carotid occlusion on lymphatic pressure. Blood was pumped to the forelimb via the brachial artery. Cannulas were placed to measure systemic, central venous, and forelimb vascular pressures. Catecholamines, whether added to the lymphatic perfusate or infused into the forelimb arterial blood, and bilateral carotid occlusion significantly increased lymphatic perfusion pressure. Perfusion of prenodal lymphatics disconnected from downstream vessels and nodes indicated that this increase occurred primarily in prenodal lymph vessels. Hemorrhagic hypotension to 55 mmHg did not affect lymphatic pressure but reduction to 35 mmHg did. The increase in lymphatic pressure produced by epinephrine and norepinephrine was blocked by phentolamine. Increased lymphatic perfusion pressure subsequent to exogenous catecholamines, severe hemorrhagic hypotension, or bilateral carotid occlusion supports the possibility that lymphatic function is modulated by adrenergic mechanisms in physiological and/or pathophysiological states.

Effect of Bilateral Occlusion of Common Carotid Arteries on Cardiac Output and Oxygen Content of Arterial and Venous Blood in the Anesthetized Dog

1956 ◽  
Vol 185 (3) ◽  
pp. 483-486 ◽  
Author(s):  
Shirley H. Brind ◽  
Joseph R. Bianchine ◽  
Matthew N. Levy
Keyword(s):  
Cardiac Output ◽  
Oxygen Content ◽  
Venous Blood ◽  
Carotid Occlusion ◽  
Systemic Hypertension ◽  
Arterial Blood ◽  
Venous Oxygen Content ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Common Carotid Arteries

Changes in cardiac output, mean arterial blood pressure, hematocrit ratio, and arterial and venous oxygen content resulting from bilateral carotid occlusion were investigated. Cardiac output exhibited no significant alteration during endosinusal hypotension, and the systemic hypertension engendered was attributed to an increase in vasomotor tone. Arterial and venous oxygen content, as well as hematocrit ratio, increased significantly during the period of carotid occlusion. This increase was ascribed to splenic contraction evoked by carotid occlusion, since no comparable augmentation was observed when the splenic circulation was temporarily interrupted.

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.

Maintained ability of carotid baroreflex to regulate arterial pressure during exercise

1981 ◽  
Vol 241 (6) ◽  
pp. H838-H849 ◽  
Author(s):  
A. Melcher ◽  
D. E. Donald
Keyword(s):  
Arterial Pressure ◽  
Work Load ◽  
Carotid Occlusion ◽  
Exercise Stress ◽  
Response Curves ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Bilateral Carotid ◽  
Bilateral Vagotomy ◽  
Cardiopulmonary Receptors

In conscious dogs bilateral carotid occlusion increased arterial pressure by similar amounts at rest (+ 27 mmHg) and during graded exercise (+ 29 mmHg). During exercise stimulus-response curves for arterial pressure and heart rate derived from isolated carotid sinuses were displaced upward proportionately to the work load, but the curve characteristics were unchanged. After acute bilateral vagotomy similar responses to carotid occlusion were obtained at rest (+ 85 mmHg) and at 21% grade (+ 84 mmHg); the range and maximal slope of the arterial pressure stimulus-response curve during exercise was similar to that at rest, but the exercise curve was displaced downward and to the left. It was concluded that the carotid baroreflex was able to modulate arterial pressure as well during running as at rest. Dogs with neither carotid, aortic, or cardiopulmonary receptors able to respond to the exercise stress became and remained hypotensive during mild exercise; during severe exercise hypotension was present initially, but after 90 s arterial pressure recovered toward the preexercise level. The data indicated that arterial and cardiopulmonary baroreceptors have a major role in the support of arterial pressure in the first moments of exercise.

Carotid arterial control of vasopressin secretion in sheep

1984 ◽  
Vol 247 (3) ◽  
pp. R589-R594 ◽  
Author(s):  
C. E. Wood ◽  
L. C. Keil ◽  
A. M. Rudolph
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Concentrations ◽  
Carotid Occlusion ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Carotid Arterial

The purpose of this study was to test the role of carotid arterial mechanoreceptors in the control of vasopressin secretion in conscious 6- to 7-wk-old lambs. Bilateral carotid occlusion decreased lingual arterial pressure and stimulated reflex increases in heart rate and femoral arterial blood pressure but did not significantly alter plasma concentrations of vasopressin. Acute vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, did not significantly alter heart rate or blood pressure but did stimulate a slow increase in plasma vasopressin concentration, suggesting that afferent vagal fibers tonically inhibit vasopressin secretion. Bilateral carotid occlusion after vagosympathetic blockade stimulated a brisk increase in plasma vasopressin that was larger than the response to vagosympathetic blockade alone. These results suggest that vasopressin secretion in lambs is partially controlled by arterial mechanoreceptors in the carotid sinus and by extracarotid receptors with vagosympathetic afferent fibers.

Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate

1989 ◽  
Vol 257 (3) ◽  
pp. R595-R598 ◽  
Author(s):  
K. G. Cornish ◽  
M. W. Barazanji ◽  
T. Yong ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Nonhuman Primate ◽  
Volume Expansion ◽  
Maximum Sensitivity ◽  
Response Curves ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Before And After ◽  
The Right

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

Fetal responses to carotid occlusion: immaturity of buffering systems

1995 ◽  
Vol 268 (2) ◽  
pp. R343-R348 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Late Gestation ◽  
Vagal Afferents ◽  
Carotid Occlusion ◽  
Fetal Sheep ◽  
Hormonal Responses ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Functional Immaturity ◽  
Vagal Afferent

In postnatal animals, carotid occlusion does not stimulate reflex hormonal responses, because decreases in carotid arterial baroreceptor activity are balanced by reflex-mediated increases in vagal afferent traffic from aortic and cardiac receptors. The present experiments were designed to test the hypothesis that hormonal responses to carotid occlusion in fetal animals are not inhibited by vagal afferents. In thirteen chronically catheterized fetal sheep (125-146 days), bilateral carotid occlusion (n = 11) increased arterial blood pressure from 44.0 +/- 2.4 to 55.2 +/- 3.3 mmHg, decreased heart rate from 189 +/- 5 to 165 +/- 12 beats/min, increased plasma adrenocorticotropin from 71 +/- 15 to 248 +/- 79 pg/ml and vasopressin from 3.0 +/- 1.0 to 7.4 +/- 2.6 pg/ml but did not significantly alter renin. Plasma hormone concentrations were not significantly altered in control (n = 7) experiments or in response to unilateral carotid occlusion (n = 4). The results of these experiments demonstrate the functional immaturity of the vagal afferent buffering systems in the late-gestation fetus compared with the postnatal animal.

Effect of thiamylal on the response to carotid occlusion and mild hemorrhage in rabbits

1984 ◽  
Vol 246 (6) ◽  
pp. H806-H810 ◽  
Author(s):  
T. Yamazaki ◽  
K. Sagawa
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Conscious State ◽  
Systemic Arterial Pressure ◽  
Carotid Occlusion ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Significant Difference ◽  
Before And After ◽  
Intact Condition

The effects of anesthesia (thiamylal, 30 mg/kg) on steady-state mean arterial pressure responses to bilateral carotid occlusion (BCO) and rapid 8% hemorrhage were studied in 11 rabbits chronically instrumented with an arterial pressure catheter and balloon occluders on the common carotid arteries. The BCO was repeated in the conscious and anesthetized states both before and after transecting the aortic nerves (AN). With the AN intact, the BCO response was an increase in mean systemic arterial pressure of 23.6 +/- 2.1 (SE) mmHg in the conscious state and 24.7 +/- 1.2 in the anesthetized state. With the AN cut (AN) BCO response was 46.2 +/- 1.7 mmHg in conscious state and 45.7 +/- 2.6 in anesthetized state. There was no significant difference in BCO response between conscious and anesthetized states, whether the AN was present or absent. The hemorrhage experiment was repeated on separate days under various conditions, including carotid sinus reflex elimination (CS). With AN intact the posthemorrhage fall in mean arterial pressure (delta MAPh) was 3.2 +/- 0.6 mmHg in the conscious state. Under anesthesia, delta MAPh was 3.4 +/- 0.6 mmHg in the AN intact condition, 7.3 +/- 0.9 in AN, and 34.5 +/- 6.8 in (AN + CS). There was no significant difference in delta MAP between the conscious and anesthetized states under the intact AN condition. We conclude that, in the rabbit, thiamylal anesthesia has little effect on the BCO response and the restoration of arterial pressure after a mild hemorrhage.

Carotid sinus reflex function in the alloxan diabetic rabbit

1979 ◽  
Vol 236 (3) ◽  
pp. H417-H421
Author(s):  
D. N. Matisoff ◽  
J. C. Lee ◽  
S. E. Downing
Keyword(s):  
Alloxan Diabetes ◽  
Carotid Sinus ◽  
Reflex Response ◽  
Bilateral Carotid Occlusion ◽  
Diabetic Rabbit ◽  
Bilateral Carotid ◽  
Before And After ◽  
Group A ◽  
Resting Tone ◽  
Group D

Baroreflex function was studied in three groups of adult rabbits. Seven animals were given alloxan (100-200 mg/kg) and became diabetic (group D) with mean blood sugar values of 348 +/- 30 mg/dl. Eight animals were given alloxan, but did not develop significant hyperglycemia (135 mg/dl) (group A). Nine controls (group C) were also studied (glucose, 101 mg/dl). All animals were anesthetized with pentobarbital (30 mg/kg). Blood pressure (BP) and heart rate (HR) responses to bilateral carotid occlusion (BCO) were measured before and after depressor nerve sectioning (DNx) and sinus nerve sectioning (SNx). Before sectioning, BCO caused a rise in BP of 30 +/- 4 mmHg in group C. 35 +/- 3 in group A, and 36 +/- 4 in group D. HR increased about 13 beats/min in each group. After DNx, resting BP increased in group C from 97 to 104 mmHg (P less than 0.005), but no change occurred in the other groups. Responses to BCO were significantly but similarly enhanced in all groups after DNx. HR did not increase in group D. Resting BP increased after SNx only in the controls (group C). Differences in BP elevation with BCO before and after SNx ("pure" reflex response) were identical, averaging about 35 mmHg. Thus, no alteration of BP or HR responses to BCO was identified in early alloxan diabetes. However, resting tone in the buffer nerves may have been less.

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