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.

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.

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.

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.

Quantification of right-to-left shunt with 99mTc-labelled albumin macroaggregates and 100% oxygen in patients with hereditary haemorrhagic telangiectasia

2002 ◽  
Vol 102 (2) ◽  
pp. 127-134 ◽  
Author(s):  
Johannes J. MAGER ◽  
Pieter ZANEN ◽  
Fred VERZIJLBERGEN ◽  
Cornelius J.J. WESTERMANN ◽  
Tjeerd HAITJEMA ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oxygen Content ◽  
Venous Blood ◽  
Alternative Methods ◽  
Mixed Venous Blood ◽  
Hereditary Haemorrhagic Telangiectasia ◽  
Shunt Fraction ◽  
Limits Of Agreement ◽  
Arterial Blood ◽  
Pulmonary Capillaries

Pulmonary arteriovenous malformations (PAVMs) are often associated with hereditary haemorrhagic telangiectasia (HHT). The quantification of right-to-left shunts in patients with PAVMs is important in diagnosis and follow up. Traditionally, this shunt is measured by the 100% oxygen method, in which the value for the arteriovenous difference in oxygen content, Cao2-Co2 (where Cao2 is the oxygen content of arterial blood and Co2 is the oxygen content of mixed venous blood) is estimated. Alternative methods consist of measurement of the systemic or renal uptake of 99mTc-labelled macroaggregates of albumin (MAA), which are trapped in pulmonary capillaries, but pass through PAVMs. We first measured Cao2-Co2 in 12 HHT patients before and after embolization of PAVMs. We obtained a mean value of 4.4ml/100ml, instead of the usual 5ml/100ml. Subsequently, we measured right-to-left shunt in 21 HHT patients using the 100% oxygen method and with two different methods involving 99mTc. We used the kidney-lung method (K/L method), in which it is assumed that the right kidney receives 10% of the cardiac output, and we also used a method with two tracers (HSA/MAA method): (1) 99mTc-labelled human serum albumin (HSA) (which passes through pulmonary capillaries) to measure the fraction of the cardiac output perfusing the kidneys, and (2) MAA to measure the shunt fraction. In 35 shunt measurements we evaluated this new technique and the K/L method, by comparing the results with those from the 100% oxygen method. There was poor agreement between the 100% oxygen method and the K/L method, with 95% limits of agreement for the shunt fraction of -15.2% to +15.2%. There was moderate agreement between the 100% oxygen method and the HSA/MAA method, with limits of agreement of -8.3% to +7.7%. We conclude that the different methods cannot replace each other, because the limits of agreement are too wide for clinical use.

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.

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.

scholarly journals Ketone bodies metabolism during ischemic and reperfusion brain injuries following bilateral occlusion of common carotid arteries in rats

2007 ◽  
Vol 22 (2) ◽  
pp. 125-129 ◽  
Author(s):  
Mário Henrique Girão Faria ◽  
Luis Roberto Franklin Muniz ◽  
Paulo Roberto Leitão de Vasconcelos
Keyword(s):  
Brain Ischemia ◽  
Alternative Energy ◽  
Wistar Rats ◽  
Carotid Arteries ◽  
Ketone Bodies ◽  
Ischemia Reperfusion ◽  
Carotid Occlusion ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Common Carotid Arteries

PURPOSE: To evaluate the in vivo alterations on ketone bodies metabolism after cerebral ischemia/reperfusion through an experimental model of brain ischemia induced by simple occlusion of common carotid arteries (CCAs) in Wistar rats. METHODS: Forty-eight male Wistar rats were randomly distributed on two groups (S - Sham; T - Test) and further redistributed into four times sets of study. After bilateral occlusion of CCAs for 30min, the animals of group T were allowed reperfusion for 0, 5, 10 and 15min. Samples of cerebral tissue and systemic arterial blood were collected and the metabolites acetoacetate (ACT) and beta-hydroxybutyrate (BHB) were determined. RESULTS: Cerebral ACT and BHB levels increased significantly in Group T after 30min of carotid occlusion (time 0). The highest brain ketone bodies (ACT+BHB) concentration was verified at 5min of reperfusion, decreasing after 10min of recirculation. Systemic ketone bodies levels increased similarly between test and sham groups. Group S demonstrated a significant increase in cerebral and systemic ACT and BHB concentrations mainly after 40-45min of study. CONCLUSIONS: The partial transient acute global brain ischemia induced by the bilateral carotid occlusion in Wistar rats triggered ketogenesis probably due to a central stimulation of catecholamine secretion. There was an increased cerebral uptake of ketone bodies following brain ischemia, reaffirming these metabolites as alternative energy substrates under conditions of cerebral metabolic stress as well as its potential role on neuroprotection. The greatest changes in ketone bodies metabolism were verified at initial minutes of recirculation as a result of the reperfusion injury phenomenon.

Hepatic Capacitance Vessel Responses to Bilateral Carotid Occlusion in Anesthetized Cats

1972 ◽  
Vol 50 (3) ◽  
pp. 244-247 ◽  
Author(s):  
W. W. Lautt ◽  
C. V. Greenway
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Baroreceptor Reflex ◽  
Carotid Occlusion ◽  
Capacitance Vessel ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Significant Difference ◽  
Hepatic Volume ◽  
The Mean

Hepatic volume was recorded by a plethysmographic technique in cats anesthetized with pentobarbital; the hepatic artery and portal vein remained intact. The mean change in hepatic blood volume during bilateral carotid occlusion was less than 2% and there was no significant difference between responses in innervated and denervated livers. These results, together with other reports in the literature, support the conclusion that capacitance vessel responses, a redistribution of blood volume, a change in cardiac output, and release of catecholamines from the adrenal medullae do not occur in arterial baroreceptor reflex responses.

Abstract P305: Sympathetic Activation Elicited by Bilateral Carotid Occlusion Attenuates Cytokine Release in Conscious Endotoxemic Rats

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Fernanda Brognara ◽  
Jaci A Castania ◽  
Daniel P Dias ◽  
Rubens Fazan ◽  
Fernando Q Cunha ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Carotid Occlusion ◽  
Saline Control ◽  
Sympathetic Activation ◽  
Conscious Rats ◽  
Bilateral Carotid Occlusion ◽  
Tnf Α ◽  
Bilateral Carotid ◽  
Saline Administration ◽  
Common Carotid Arteries

Our previous studies suggest that carotid occlusion can induce a sympathetic signal able to modulate the immune system. Here, we analyze whether bilateral carotid occlusion (BCO) affect the innate immune response to bacterial lipopolysaccharide (LPS) in endotoxic rats. In order to prevent the neuronal alterations induced by anesthesia, we performed our studies of BCO in conscious rats. Wistar rats were implanted with pneumatic cuffs around the common carotid arteries for BCO. Femoral and peritoneal catheters were also inserted for blood pressure recording and LPS administration. Rats were randomly assigned to the following groups: Saline, LPS + SHAM (LPS in the presence of the occluders but without occlusion) and LPS + BCO (LPS combined with bilateral carotid occlusion). BCO was performed for 20s in conscious awake rats, right before LPS (5.0 mg/kg) or saline (control) administration. Plasma and spleen samples were collected at 90 min after LPS or saline administration. As compared to baseline arterial pressure, BCO produced a peak response in mean arterial pressure of 52 ± 3 mmHg, confirming the sympathetic activation. BCO significantly attenuated TNF-α and IL-1β plasma levels as compared to those in SHAM endotoxemic rats [TNF: 1319 ± 388 (n = 6) vs. 583 ± 138 pg/mL (n = 8), P = 0.03; IL-1β: 2203 ± 256 (n = 5) vs. 1086 ± 157 pg/mL (n = 9), P < 0.001]. BCO also significantly reduced the TNF-α levels in the spleen [5.1 ± 1.3 (n = 7) vs. 1.7 ± 0.4 pg/mg tissue (n = 8), P = 0.005]. By contrast, BCO did not significantly change IL-6 and IL-10 levels in plasma [IL-6: 5609 ± 352 (n = 7) vs. 5879 ± 375 pg/mL (n = 10), P = 0.703; IL-10: 2417 ± 354 (n = 5) vs. 2068 ± 298 pg/mL (n = 9), P = 0.408] or in the spleen [IL-6: 15 ± 3 (n = 7) vs. 14 ± 2 pg/mg tissue (n = 10) P = 0.776; IL-10: 1.6 ± 0.2 (n = 7) vs. 1.3 ± 0.2 pg/mg tissue (n = 9), P = 0.475]. Moreover, the IL-1β level in the spleen was not affected by BCO [54 ± 12 (n = 6) vs. 28 ± 5 pg/mg tissue (n = 9), P = 0.058]. These findings indicate that sympathetic activation by BCO in conscious rats attenuates the pro-inflammatory cytokines release in the endotoxemic model induced by LPS without affecting anti-inflammatory cytokine IL-10.

Sign in / Sign up

Export Citation Format

Share Document