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.

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.

scholarly journals Physiological Sympathetic Activation Reduces Systemic Inflammation: Role of Baroreflex and Chemoreflex

2021 ◽  
Vol 12 ◽  
Author(s):  
Fernanda Brognara ◽  
Jaci Airton Castania ◽  
Alexandre Kanashiro ◽  
Daniel Penteado Martins Dias ◽  
Helio Cesar Salgado
Keyword(s):  
Nervous System ◽  
Arterial Pressure ◽  
Systemic Inflammation ◽  
Inflammatory Responses ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Sympathetic Activation ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Reflex Activation

Baroreflex and chemoreflex act through the autonomic nervous system, which is involved with the neural regulation of inflammation. The present study reports the effects of reflex physiological sympathetic activation in endotoxemic rats using bilateral carotid occlusion (BCO), a physiological approach involving the baroreflex and chemoreflex mechanisms and the influence of the baroreceptors and peripheral chemoreceptors in the cardiovascular and systemic inflammatory responses. After lipopolysaccharide (LPS) administration, the arterial pressure was recorded during 360 min in unanesthetized rats, and serial blood samples were collected to analyze the plasma cytokine levels. BCO elicited the reflex activation of the sympathetic nervous system, providing the following outcomes: (I) increased the power of the low-frequency band in the spectrum of the systolic arterial pressure during the BCO period; (II) reduced the levels of pro-inflammatory cytokines in plasma, including the tumor necrosis factor (TNF) and the interleukin (IL)-1β; (III) increased the plasma levels of anti-inflammatory cytokine IL-10, 90 min after LPS administration. Moreover, selective baroreceptor or chemoreceptor denervation deactivated mechanosensitive and chemical sensors, respectively, and decreased the release of the LPS-induced cytokine but did not alter the BCO modulatory effects. These results show, for the first time, that physiological reflex activation of the sympathetic circuit decreases the inflammatory response in endotoxemic rats and suggest a novel function for the baroreceptors as immunosensors during the systemic inflammation.

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.

The effects of forebrain multiple lesions on the pressor response induced by bilateral carotid occlusion in conscious rats

1993 ◽  
Vol 612 (1-2) ◽  
pp. 243-246 ◽  
Author(s):  
Maria Tereza Barbieri Bedran de Castro ◽  
Joa˜o Cesar Bedran de Castro ◽  
Jose´Vanderlei Menani
Keyword(s):  
Pressor Response ◽  
Carotid Occlusion ◽  
Conscious Rats ◽  
Multiple Lesions ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

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.

Central antihypertensive properties of muscimol and related γ-aminobutyric acid agonists and the interaction of muscimol with baroreceptor reflexes

1979 ◽  
Vol 57 (6) ◽  
pp. 600-605 ◽  
Author(s):  
Charles S. Sweet ◽  
Herbert C. Wenger ◽  
Dennis M. Gross
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Dose ◽  
Carotid Occlusion ◽  
Aminobutyric Acid ◽  
Intracerebroventricular Infusion ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Baroreceptor Reflexes ◽  
Antihypertensive Properties

The central antihypertensive properties of four γ-aminobutyric acid (GABA) analogs were characterized in anesthetized cats with implanted intracerebroventricular cannulae. An intracerebroventricular infusion (icv) of muscimol, 0.1–0.5 μg/min (total dose: 1–5 μg, icv), substantially reduced mean arterial pressure and slightly reduced heart rate. The compound was not hypotensive at 5 μg, iv (total dose) and only slightly hypotensive after an intracisternal injection (5 μg). Kojic amine (2-aminomethyl-5-hydroxy-4H-pyran-4-one) and baclofen were also hypotensive following an intracerebroventricular infusion, but they were less active than muscimol. GABA, at 15–150 μg/min, icv (total dose, 150–1500 μg, icv), was not hypotensive by itself and unlike muscimol its activity was not enhanced in cats pretreated with nipecotic acid, an uptake inhibitor of GABA. The ability of muscimol to interfere with baroreceptor reflexes was considered in experiments in which reflex vasoconstrictor (carotid occlusion) and reflex vasodilatation (acute elevation in mean arterial pressure with norepinephrine) was measured in the perfused hindlimb of cats previously prepared with intracerebroventricular cannulae. Muscimol significantly attenuated the response to bilateral carotid occlusion and completely abolished reflex vasodilatation. These results suggest that GABA agonists and analogs may regulate blood pressure centrally and, through an interaction with the central nervous system, may attenuate baroreceptor reflexes.

Role of parabrachial nucleus in baroreflex-mediated coronary vasoconstriction

1996 ◽  
Vol 271 (3) ◽  
pp. H1079-H1086 ◽  
Author(s):  
D. D. Gutterman ◽  
A. Goodson
Keyword(s):  
Arterial Pressure ◽  
Kainic Acid ◽  
Coronary Flow ◽  
Carotid Occlusion ◽  
Parabrachial Nucleus ◽  
Coronary Vasoconstriction ◽  
Coronary Constriction ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

Coronary vasoconstriction is a component of the baroreflex response to bilateral carotid occlusion. The central pathways responsible for this reflex constriction are incompletely understood, but previous studies show that activation of parabrachial nucleus (PBN) elicits coronary vasoconstriction and that PBN shares prominent anatomic connections with other central baroreflex centers, including the nucleus of the tractus solitarius. Therefore, we examined whether PBN plays a role in baroreflex mediated coronary constriction and whether cell bodies rather than fibers passing through this region are involved. Anesthetized cats were instrumented for continuous measurements of heart rate, arterial pressure, and coronary flow velocity. Bilateral carotid occlusion following propranolol and vagotomy increased arterial pressure (63 +/- 10%) and an index of coronary vascular resistance (34 +/- 6%). Bilateral microinjections of lidocaine (1%, 400 nl) into PBN reversibly attenuated the coronary constriction (19 +/- 5%) with little effect on the change in arterial pressure. It was further demonstrated that autoregulatory responses to the increase in pressure could not fully account for the observed changes in coronary constriction. In a separate group of animals, kainic acid (50 mM, 300 nl) abolished the baroreflex increase in coronary resistance (43 +/- 1 vs. -9 +/- 9% after) without affecting the increase in arterial pressure (54 +/- 12% increase before vs. 55 +/- 20% increase after kainic acid). We conclude that PBN is a necessary component of the baroreflex pathway mediating coronary vasoconstriction. Furthermore, cell bodies in PBN, rather than simply fibers passing through that region, participate in the reflex coronary vasoconstriction.

Severe Hypotension Is Not Essential for Isoflurane Neuroprotection against Forebrain Ischemia in Mice

2003 ◽  
Vol 99 (5) ◽  
pp. 1145-1151 ◽  
Author(s):  
H. Mayumi Homi ◽  
Javier M. Mixco ◽  
Huaxin Sheng ◽  
Hilary P. Grocott ◽  
Robert D. Pearlstein ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Occlusion ◽  
Plasma Norepinephrine ◽  
Ischemic Insult ◽  
Bilateral Carotid Occlusion ◽  
Severe Hypotension ◽  
Bilateral Carotid ◽  
Neurologic Function

Background Volatile anesthetics provide protection in experimental models of global cerebral ischemia. To date, all models evaluated have included profound systemic arterial hypotension as a component of the ischemic insult. This study was designed to determine if isoflurane protection persists in a global insult devoid of hypotension. Methods C57BL/6J mice having a high incidence of posterior communicating artery atresia were anesthetized with isoflurane (1.2%) or fentanyl/N2O and subjected to bilateral carotid artery occlusion for 15 min or 20 min with normotension (80-110 mmHg mean arterial pressure) or for 10 min with hypotension (35 mmHg mean arterial pressure). Three days later, neurologic function and histologic damage were assessed. Other mice underwent measurement of intraischemic cerebral blood flow (4-iodo-N-methyl-[14C]antipyrine autoradiography) or plasma norepinephrine. Results Isoflurane reduced the percentage of hippocampal CA1 dead neurons (e.g., 10 min bilateral carotid occlusion + hypotension: 43 +/- 18 (isoflurane) vs. 67 +/- 20 (fentanyl/N2O), P = 0.003; 20 min bilateral carotid occlusion + normotension: 49 +/- 27 (isoflurane) vs. 71 +/- 22 (fentanyl/N2O), P = 0.003). Isoflurane also reduced CA3 damage and improved neurologic function under all conditions. Intraischemic forebrain blood flow was similar during bilateral carotid occlusion plus normotension for the two anesthetic states. Plasma norepinephrine values were greater when hypotension was added to the ischemic insult. Conclusions Isoflurane resulted in improved neurologic function and reduced histologic damage regardless of the presence or absence of systemic hypotension during the ischemic insult. This indicates that beneficial effects of isoflurane are most likely attributable to direct effects at the neuronal level as opposed to indirect effects resulting from interactions with profound hypotension.

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