Sudden coma onset following simultaneous bilateral carotid occlusion

Author(s):  
Géraud Forestier ◽  
Antoine Dusonchet ◽  
François Lun ◽  
Grégoire Boulouis
1992 ◽  
Vol 72 (4) ◽  
pp. 1247-1254 ◽  
Author(s):  
J. M. Lash ◽  
E. Haase ◽  
A. A. Shoukas

We evaluated the effects of four standard anesthetization regimens on the systemic cardiovascular responses to bilateral common carotid artery occlusion in 28 adult male rats. Rats were randomly assigned to anesthesia groups: thiopental sodium (PT; 100 mg/kg ip), alpha-chloralose (CH; 100 mg/kg iv), ketamine hydrochloride plus acepromazine (KA; 135 mg/kg and 1.5 mg/kg sc), and pentobarbital sodium (PB; 50 mg/kg ip). PT and PB animals had similar baseline heart rates (HR; 333 and 345 beats/min, respectively) and arterial pressures (MAP; 126 and 118 mmHg, respectively), whereas both were lower in CH and KA (314 and 288 beats/min, 92 and 85 mmHg). During bilateral carotid occlusion, PT demonstrated the largest change in MAP (dMAP; +27 mmHg) but the smallest change in HR (dHR; +8 beats/min). CH and PB demonstrated similar dHR (+24 and +16 beats/min) and dMAP (+20 and +19 mmHg). KA demonstrated a significant dHR (+14 beats/min), but the average dMAP was not statistically significant (+3 mmHg). Therefore, carotid occlusion in rats anesthetized with PT, PB, or CH consistently elicits a systemic arterial pressor response comparable with that reported for conscious animals. When the magnitude and stability of baseline HR and MAP are also considered, PT and PB anesthetization seem to be the most reliable for evaluation of the carotid occlusion pressor response in rats.


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

1988 ◽  
Vol 255 (3) ◽  
pp. H514-H524
Author(s):  
J. M. Dabney ◽  
M. J. Buehn ◽  
D. E. Dobbins

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.


1990 ◽  
Vol 258 (3) ◽  
pp. R624-R633 ◽  
Author(s):  
D. E. Fitzovich ◽  
D. C. Randall

We developed a conscious, chronically instrumented canine preparation (n = 5 dogs) in which insulin concentration was precisely controlled to study the effects of controlled variations of plasma insulin and glucose concentrations on cardiac responses to bilateral carotid occlusion and dobutamine. Endogenous insulin secretion was reduced to negligible levels using alloxan and then replaced by continuous, constant intravenous insulin infusion at a rate (0.625 +/- 0.115 U/h) sufficient to maintain fasting normoglycemia (85 +/- 9 mg/100 ml); plasma immunoreactive insulin (IRI) in this basal "normal insulin, normal glucose" (NI,NG) condition was 0.362 +/- 0.45 ng/ml (NS vs. prealloxan fasting concentration). A fivefold increase of IRI from NI,NG levels with normoglycemia maintained (5 x NI,NG) reduced (P less than 0.05) the maximal first time derivative of left ventricular pressure (LV dP/dtmax) from 3,010 +/- 62 to 2,398 +/- 91 (SE) mmHg/s but had no effect on LV dP/dtmax when plasma glucose was elevated to 298 +/- 25 mg/100 ml (5 x NI,HG). The LV dP/dtmax increase during bilateral carotid occlusion (BCO) in the NI,NG state of 124 +/- 17 mmHg/s was significantly reduced (P less than 0.05) in the 5 x NI,HG state to 58 +/- 18 mmHg/s but was not altered in the 5 x NI,NG state. Reduction of plasma insulin to one-fifth of the normal fasting level had no effect on basal cardiac function or the responses to BCO. There were no other statistically significant effects of insulin or glucose concentration on cardiovascular responses to BCO or to infusion of dobutamine. Our data indicate that physiologically realistic variations in plasma IRI and glucose concentrations interact and may modulate cardiovascular responses to changes in autonomic nervous activity, even though previously reported effects of pharmacological doses of insulin were not observed.


1956 ◽  
Vol 185 (3) ◽  
pp. 483-486 ◽  
Author(s):  
Shirley H. Brind ◽  
Joseph R. Bianchine ◽  
Matthew N. Levy

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.


2010 ◽  
Vol 299 (6) ◽  
pp. H1990-H1995 ◽  
Author(s):  
R. M. Lataro ◽  
J. A. Castania ◽  
M. W. Chapleau ◽  
H. C. Salgado ◽  
R. Fazan

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.


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