Systemic responses to carotid occlusion in the anesthetized rat

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.

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

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1983.27 ◽

1983 ◽

Vol 3 (2) ◽

pp. 200-206 ◽

Cited By ~ 23

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.

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The Effects of Halothane on Cardiovascular Responses in the Neuraxis of Cats

Anesthesiology ◽

10.1097/00000542-199501000-00020 ◽

1995 ◽

Vol 82 (1) ◽

pp. 153-165 ◽

Cited By ~ 15

Author(s):

Neil E. Farber ◽

Enric Samso ◽

John P. Kampine ◽

William T. Schmeling

Keyword(s):

Arterial Pressure ◽

Reticular Formation ◽

Cardiovascular Responses ◽

Artery Occlusion ◽

Carotid Artery Occlusion ◽

Implanted Electrodes ◽

Bilateral Carotid Occlusion ◽

Pressor Responses ◽

Bilateral Carotid ◽

Cns Stimulation

Background This study examined the effects of halothane on arterial pressure after central nervous system (CNS) pressor site stimulation in anesthetized cats, cats rendered unconscious by midcollicular transection, and conscious cats. Methods Two anesthetized groups and two nonanesthetized groups were used. Cats were anesthetized with either alpha-chloralose and urethane or pentobarbital. Nonanesthetized groups were cats with midcollicular transections or conscious cats with chronically implanted electrodes. Stimulating electrodes were placed into vasomotor areas of the hypothalamus (HYP), reticular formation (RF), and medulla, and arterial pressure responses to increasing stimulus currents were examined during different halothane concentrations. Two groups of cats were also anesthetized with either pentobarbital or urethane and underwent bilateral carotid artery occlusion. Results Stimulation at each CNS site produced increases in arterial pressure and heart rate. Halothane attenuated pressor responses evoked by stimulation of all loci in all groups of cats. The inhibition by halothane on these cardiovascular responses was greatest at HYP and RF sites, while the medulla was more resistant to the effects of halothane in the anesthetized animals. Midcollicular transection decreased this medullary resistance. The inhibition of pressor responses by halothane was also greater in pentobarbital-than chloralose urethane-anesthetized animals. In contrast, pressor responses elicited by bilateral carotid occlusion were attenuated by halothane similarly in both anesthetic groups. Reticular formation stimulation in conscious animals resulted in "altering responses" in addition to pressor effects, both of which were attenuated by halothane. Conclusions Modulation of CNS cardiovascular control centers contribute to halothane-induced hemodynamic alterations. Baseline anesthesia, CNS stimulation site, and the suprabulbar system influence the effects of halothane.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1986.251.5.h991 ◽

1986 ◽

Vol 251 (5) ◽

pp. H991-H999 ◽

Cited By ~ 2

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.

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