Lack of liver vascular response to carotid occlusion in mildly acidotic dogs

1986 ◽  
Vol 251 (5) ◽  
pp. H991-H999 ◽  
Author(s):  
C. A. Goresky ◽  
D. Cousineau ◽  
C. P. Rose ◽  
S. Lee
Keyword(s):  
Hepatic Vein ◽  
Pressor Response ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Carotid Occlusion ◽  
Sympathetic Activation ◽  
Multiple Indicator Dilution ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Cellular Water

The effect of mild acidosis on the reduction in liver vascular volume provoked by reflex sympathetic activation was ascertained in dogs by use of the multiple indicator-dilution technique. Portal vein-hepatic vein dilution patterns were obtained following injection of a mixture containing 51Cr-labeled red blood cells (a vascular reference), 14C-labeled sucrose (an interstitial reference), and 3H-labeled water (a cellular reference). Liver vascular, interstitial, and cellular water spaces were measured in normal and mildly acidotic dogs under basal conditions and during bilateral carotid artery occlusion. Carotid occlusion resulted in a large increase in arterial blood pressure in normal and a lesser increase in acidotic dogs, but the increase in portal and hepatic vein norepinephrine and decrease in liver vascular and interstitial volumes observed in normal dogs did not occur in the acidotic animals; no change in labeled water accessible liver cellular spaces was perceptible. The data indicate that mild acidosis abolishes the ordinarily expected reduction in liver vascular volumes on sympathetic activation in the intact dog but not the arterial pressor response.

Systemic responses to carotid occlusion in the anesthetized rat

1992 ◽  
Vol 72 (4) ◽  
pp. 1247-1254 ◽  
Author(s):  
J. M. Lash ◽  
E. Haase ◽  
A. A. Shoukas
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Carotid Occlusion ◽  
Male Rats ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Common Carotid Artery ◽  
Bilateral Carotid ◽  
Common Carotid Artery Occlusion

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.

scholarly journals Ischemia Reduces Blood-to-Brain Glucose Transport in the Gerbil

1983 ◽  
Vol 3 (2) ◽  
pp. 200-206 ◽  
Author(s):  
A. Lorris Betz ◽  
Fausto Iannotti ◽  
Julian T. Hoff
Keyword(s):  
Cerebral Cortex ◽  
Basal Ganglia ◽  
Carotid Artery ◽  
Glucose Transport ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Carotid Occlusion ◽  
Brain Glucose ◽  
Bilateral Carotid ◽  
Common Carotid Artery Occlusion

The effect of carotid occlusion on cerebral blood flow (CBF), brain plasma volume for sucrose ( Vplsuc), and unidirectional transport of glucose from blood to brain was measured in four regions of gerbil brain. Unilateral common carotid artery occlusion caused a variable decrease in CBF to the ipsilateral cerebral cortex and basal ganglia, with no change in CBF to the contralateral structures, cerebellum, or brainstem. One hour of bilateral carotid artery occlusion reduced flow to near zero in the cerebral cortex and to 30% of control in the basal ganglia, while increasing CBF to the cerebellum and brainstem. There was a significant decrease in the Vplsuc of the cerebral cortex and basal ganglia after 1 h of ischemia, perhaps due to compression of the intravascular space by edema fluid. Blood-to-brain glucose transport, 1 min after release from 1 h of bilateral carotid occlusion, was decreased in the cerebral cortex and basal ganglia, but not in the cerebellum or brainstem. These data indicate that 1 h of complete or incomplete ischemia reduces the rate of unidirectional glucose transport from blood to brain.

Plasma and lymph dopamine-beta-hydroxylase and norepinephrine during carotid occlusion

1979 ◽  
Vol 236 (1) ◽  
pp. H96-H100
Author(s):  
M. T. Velasquez ◽  
N. Alexander
Keyword(s):  
General Circulation ◽  
Hepatic Clearance ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Sympathetic Activation ◽  
Peak Response ◽  
Intestinal Lymph ◽  
Arterial Blood ◽  
Dopamine Beta Hydroxylase ◽  
Venous Plasma

Dopamine-beta-hydroxylase (DBH) and norepinephrine (NE) levels in superior mesenteric venous (SMV) and arterial blood and in intestinal lymph were determined sequentially before and during carotid artery occlusion (CAO) in anesthetized rabbits. During the first 15 min of CAO, SMV plasma NE increased 77% but SMV plasma DBH increased only 11%. During the second 15 min of CAO, SMV NE declined to 36% above control but SMV DBH rose further and peaked to 29% above control after CAO was released; arterial DBH and NE showed small insignificant changes. Lymph DBH and NE increased simultaneously throughout the period of CAO. Increases in mean arterial pressure during CAO correlated with superior mesenteric venous NE (r = 0.58, P less than 0.01). In additional experiments, hepatic vein plasma NE was 74% lower than portal vein NE. Thus, during acute sympathetic activation, DBH and NE increase in mesenteric venous plasma and intestinal lymph but the peak response of plasma DBH lags behind that of NE. The degree of NE change in the general circulation is minimized due to hepatic clearance of NE.

Time course of recovery of arterial pressure control after carotid denervation

1990 ◽  
Vol 258 (1) ◽  
pp. H73-H79 ◽  
Author(s):  
D. S. O'Leary ◽  
A. M. Scher
Keyword(s):  
Arterial Pressure ◽  
Time Course ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Pressure Control ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Atrial Rate ◽  
Bilateral Carotid ◽  
Pressure Changes

We examined the recovery of arterial pressure control after carotid sinus baroreceptor denervation in conscious dogs with atrioventricular block. Strength of control was assessed by measuring changes in peripheral resistance and atrial rate after step changes in cardiac output. One day after carotid denervation, arterial pressure was significantly elevated (+13.7 mmHg), and the strength of control of peripheral resistance and atrial rate were significantly decreased to 46.1 and 36.6% of control, respectively. Over 4–7 days, the strength of control of both peripheral resistance and atrial rate and the mean arterial pressure returned to the levels observed before denervation. After carotid denervation, the pressor response to bilateral carotid artery occlusion was abolished, and thus the recovery of arterial pressure control was not caused by inadequate carotid denervation or regeneration of carotid baroreceptors. The recovery of arterial pressure control after carotid denervation is probably caused by an increase in the reflex responses to pressure changes at the aortic baroreceptors and may reflect plasticity within the baroreflex pathway.

scholarly journals Assessment of Postischemic Neurogenesis in Rats with Cerebral Ischemia and Propofol Anesthesia

2009 ◽  
Vol 110 (3) ◽  
pp. 529-537 ◽  
Author(s):  
Irina Lasarzik ◽  
Uta Winkelheide ◽  
Sonja Stallmann ◽  
Christian Orth ◽  
Astrid Schneider ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Spatial Learning ◽  
Neuronal Damage ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
High Dose ◽  
Sprague Dawley ◽  
Bilateral Carotid ◽  
Significant Difference ◽  
Treatment Naïve

Background Postischemic endogenous neurogenesis can be dose-dependently modulated by volatile anesthetics. The intravenous anesthetic propofol is used during operations with a risk of cerebral ischemia, such as neurosurgery, cardiac surgery, and vascular surgery. The effects of propofol on neurogenesis are unknown and, therefore, the object of this study. Methods Eighty male Sprague-Dawley rats were randomly assigned to treatment groups with propofol administration for 3 h: 36 mg x kg(-1) x h(-1) propofol with or without cerebral ischemia and 72 mg x kg(-1) x h(-1) propofol with or without cerebral ischemia. In addition, 7 rats with propofol administration for 6 h and 14 treatment-naive rats were investigated. Forebrain ischemia was induced by bilateral carotid artery occlusion and hemorrhagic hypotension. Animals received 5-bromo-2-deoxyuridine for 7 days. 5-Bromo-2-deoxyuridine-positive neurons were counted in the dentate gyrus after 9 and 28 days. Spatial learning in the Barnes maze and histopathologic damage of the hippocampus were analyzed. Results Propofol revealed no impact on basal neurogenesis. Cerebral ischemia increased the amount of new neurons. After 28 days, neurogenesis significantly increased in animals with low-dose propofol administered during cerebral ischemia compared with naive animals, whereas no significant difference was observed in animals with high-dose propofol during ischemia. Neuronal damage in the CA3 region was increased at 28 days with high-dose propofol. Postischemic deficits in spatial learning were not affected by propofol. Conclusions Independent effects of propofol are difficult to ascertain. Peri-ischemic propofol administration may exert secondary effects on neurogenesis by modulating the severity of histopathologic injury and thereby regenerative capacity of the hippocampus.

Assessing the Effects of Antihypertensive Medication on Cerebral Blood Flow: Demonstration in Internal Carotid Artery Occlusion

DICP ◽  
1991 ◽  
Vol 25 (12) ◽  
pp. 1299-1301 ◽  
Author(s):  
Susan C. Fagan ◽  
James R. Ewing ◽  
Steven R. Levine ◽  
Gretchen E. Tietjen ◽  
Nabih M. Ramadan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Antihypertensive Medication ◽  
Internal Carotid ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Internal Carotid Artery Occlusion ◽  
Bilateral Carotid

Dynamic cerebral blood flow (CBF) studies using acetazolamide or hypercapnia as a vasodilatory challenge have attempted to evaluate intracranial hemodynamics. We report two patients with asymptomatic internal carotid artery occlusion in whom the vasodilatory stimulus was a single oral dose of antihypertensive medication (prazosin hydrochloride or enalapril maléate). In both patients, changes in regional CBF occurred that were larger than those seen in nine normal controls. One patient experienced an improvement in regional CBF with a reduction in probe pair asymmetry. In the other patient, who had bilateral carotid artery disease, a decrease in regional CBF in all 16 probes (mean decrease 12 percent) and an accentuation of the predose asymmetry were observed. Both patients remained asymptomatic throughout the study. Assessing these effects on cerebral circulation may help identify patients at risk for iatrogenic focal cerebral ischemia and provide information regarding the functional status of the cerebral vasculature.

Abstract WP33: Reperfusion Therapy in Carotid Artery Occlusion with Collaterals Through the Circle of Willis

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Seong Hwan Ahn ◽  
In Sung Choo ◽  
Hyun Gu Kang ◽  
Ji Yeon Jung ◽  
Sang Woo Ha
Keyword(s):  
Carotid Artery ◽  
Endovascular Treatment ◽  
Recurrent Stroke ◽  
Reperfusion Therapy ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Circle Of Willis ◽  
Carotid Occlusion ◽  
Large Artery ◽  
Clinical Worsening

Introduction: In large artery occlusion, endovascular treatment shows better recanalization rate than intravenous tPA alone. In reperfusion therapy, excellent collaterals through the circle of Willis has better prognosis. We hypothesized that intravenous tPA only is comparable to endovascular therapy in carotid occlusion with patent ‘T’. Methods: Between January 2010 and December 2015, in acute stroke patients who had received a reperfusion therapy, carotid artery occlusion with good collateral via the circle of Willis were selected. In all patients, non-contrast CT and CT angiography were conducted before reperfusion therapy and at 24 (+/-6) hours and/or clinical worsening. Stroke severity was assessed with NIHSS at baseline and discharge. The prognosis of reperfusion therapy was assessed by modified Rankin Scales at 3 months. Results: In 529 patients treated by reperfusion therapy, 29 patients (5.5%, male 21, median age 76) had internal carotid artery occlusion with patent ‘T’. In tPA alone (24 patients, 82.8%), baseline NIHSS were non-significantly lower than in endovascular treatment (10 vs 15, p=0.224). Recurrent stroke, which was confirmed with follow up angiography, was developed in 8 of tPA alone. In endovascular treatment, one had a distal embolization. In 22 patients who could be assessed by MRS, 10 patients (45.5%, tPA in 9, IA in 1) had good mRS and 6 patients (27.3%) were expired. Conclusions: Carotid occlusion with good collaterals via the circle of Willis was uncommon. tPA alone resulted in recurrent stroke with clinical worsening. Endovascular treatment may be better option in carotid occlusion with patent ‘T’.

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