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.

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.

scholarly journals Neuroprotective Effects of Bone Marrow Mesenchymal Stem Cells on Bilateral Common Carotid Arteries Occlusion Model of Cerebral Ischemia in Rat

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Bagher Pourheydar ◽  
Sara Soleimani Asl ◽  
Mostafa Azimzadeh ◽  
Adel Rezaei Moghadam ◽  
Asghar Marzban ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cerebral Ischemia ◽  
Functional Recovery ◽  
Carotid Arteries ◽  
Ischemia Reperfusion ◽  
Neuroprotective Effects ◽  
Marrow Mesenchymal Stem Cells ◽  
Common Carotid Arteries

Cell therapy is the most advanced treatment of the cerebral ischemia, nowadays. Herein, we discuss the neuroprotective effects of bone marrow mesenchymal stem cells (BMSCs) on rat hippocampal cells following intravenous injection of these cells in an ischemia-reperfusion model. Adult male Wistar rats were divided into 5 groups: control, sham (surgery without blockage of common carotid arteries), ischemia (common carotid arteries were blocked for 30 min prior to reperfusion), vehicle (7 days after ischemia PBS was injected via the tail vein), and treatment (injections of BMSC into the tail veins 7 days after ischemia). We performed neuromuscular and vestibulomotor function tests to assess behavioral function and, finally, brains were subjected to hematoxylin and eosin (H&E), anti-Brdu immunohistochemistry, and TUNEL staining. The ischemia group had severe apoptosis. The group treated with BMSCs had a lower mortality rate and also had significant improvement in functional recovery (P<0.001). Ischemia-reperfusion for 30 min causes damage and extensive neuronal death in the hippocampus, especially in CA1 and CA3 regions, leading to several functional and neurological deficits. In conclusion, intravenous injection of BMSCs can significantly decrease the number of apoptotic neurons and significantly improve functional recovery, which may be a beneficial treatment method for ischemic injuries.

scholarly journals Severe autogenously fecal peritonitis in Wistar rats with permanent bilateral carotid occlusion. Response to intra peritoneal moxifloxacin combined with dexamethasone

2014 ◽  
Vol 29 (2) ◽  
pp. 76-81 ◽  
Author(s):  
Maria Cecília Santos Cavalcanti Melo ◽  
Diego Nery Benevides Gadelha ◽  
Thárcia Kiara Beserra Oliveira ◽  
Carlos Teixeira Brandt
Keyword(s):  
Wistar Rats ◽  
Carotid Occlusion ◽  
Fecal Peritonitis ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

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.

Respiratory sensitivity to carbon dioxide in cross-circulated dogs

1962 ◽  
Vol 202 (5) ◽  
pp. 1024-1028 ◽  
Author(s):  
Frederick F. Kao ◽  
Remedios G. Suntay ◽  
William K. Li
Keyword(s):  
Carbon Dioxide ◽  
Carotid Arteries ◽  
Ventilatory Response ◽  
Sensitivity Coefficient ◽  
Vertebral Arteries ◽  
Arterial Blood ◽  
The Common ◽  
Respiratory Centers ◽  
Common Carotid Arteries ◽  
Respiratory Sensitivity

The effect of CO2 on ventilation was studied in cross-circulated dogs. In these experiments the recipient dog's head was perfused exclusively by arterial blood from the donor dog through anastomoses of the common carotid arteries of the donor to the vertebral arteries of the recipient. The carotid arteries of the recipient dog, as well as its muscles in the neck, were tied. The injection of lipiodol and latex did not reveal leakage from the recipient's head to its body or vice versa. Ventilation and arterial Pco2 of both dogs were determined before, during, and after the inhalation of carbon dioxide of 3, 5, and 7% with 20% oxygen and balance nitrogen by the donor for 20 min or more. The sensitivity of the respiratory centers of both dogs to Pco2 was similar, as indicated by the regression lines relating ventilation in both dogs as a function of arterial Pco2 of the donor dog only. The blood of the recipient's body was hypocapnic when its head was receiving hypercapnic blood. The sensitivity coefficient in both dogs was similar to that of decerebrate dogs during CO2 inhalation. It is inferred that the central CO2 chemoreceptors can account for all the ventilatory response to CO2 inhalation.

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.

Effects of Bilateral Vagotomy on Renal Function in the Rat

1971 ◽  
Vol 49 (5) ◽  
pp. 420-426 ◽  
Author(s):  
Paul F. Mercer
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Carotid Arteries ◽  
Control Group ◽  
Vagus Nerves ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Common Carotid Arteries

Renal function was studied in rats before and after section of the vagus nerves at the level of the common carotid arteries. In the control group of rats, sodium output and volume rate of urine flow increased following vagal section but glomerular filtration rate did not change. This response was not altered in other rats by desoxycorticosterone acetate, vasopressin, or renal nerve section. This response was similar to that seen in rats in which both common carotid arteries had been occluded. The natriuresis following bilateral vagotomy did not occur in rats in which the blood pressure was prevented from rising by means of aortic constriction. It is concluded that a natriuresis does occur following bilateral vagotomy. This natriuresis may be a result of the effect of arterial blood pressure following the vagotomy.

scholarly journals Autoregulation in the Middle Meningeal Artery

1996 ◽  
Vol 16 (3) ◽  
pp. 507-516 ◽  
Author(s):  
J. Michalicek ◽  
V. Gordon ◽  
G. Lambert
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Arteries ◽  
Middle Meningeal Artery ◽  
Gain Factor ◽  
Arterial Blood ◽  
Neuronal Mechanisms ◽  
Flow Through ◽  
Common Carotid Arteries ◽  
Meningeal Artery

In cats anesthetized with α-chloralose, auto-regulation of blood flow (F) in the middle meningeal and common carotid arteries was assessed by bleeding and subsequently reinfusing the animals to achieve a 25% step reduction in mean arterial blood pressure (P), while maintaining the systolic blood pressure >80 mmHg. The integrity of autoregulation was assessed by calculating the gain factor Gf = 1 — [(ΔF/F)/(ΔP/P)]. Cats were examined intact, after hexamethonium (10 mg/kg), and after papaverine (6 mg/kg). Reduction of blood pressure of 25 to 60 mmHg produced equivalent drops in carotid blood flow ( Gf = 0.041 ± 0.34; mean ± standard deviation, n = 12). There were only small changes in flow in the middle meningeal artery during this procedure ( Gf = 0.91 ± 0.29). Hexamethonium did not block autoregulation in the middle meningeal artery ( Gf = 0.92 ± 0.13, n = 4). However, papaverine almost completely abolished the ability of the artery to autoregulate ( Gf = 0.10 ± 0.16, n = 7). The results suggest that the middle meningeal artery possesses an ability similar to that of the cortical circulation to autoregulate its blood flow through intrinsic, non-neuronal mechanisms. This will have important implications for the study of disturbances of dural arterial control in migraine and other headaches.

Sign in / Sign up

Export Citation Format

Share Document