The Glucose Content of Brain in Anaesthesia*

Mayman, Chaim I.; Gatfield, P. D.; Breckenridge, Bruce McL.

doi:10.1111/j.1471-4159.1964.tb11607.x

Cited by 127 publications

(29 citation statements)

References 8 publications

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“…Table III compares the present data with comparable published data. It is likely that the difference between the present results and those of Lowry et al (9)(10)(11) are largely due to the smaller head size in the mouse and differences in freezing technique.…”

Section: Resultscontrasting

confidence: 55%

“…It is of interest to compare these observations with the known effects of anesthesia (10). A high level of labile phosphate sustained after decapitation and a diminished glycolytic response to ischemia are features of both uremia and anesthesia.…”

Section: Resultsmentioning

confidence: 99%

“…The high brain glucose in the uremic rat merely reflects the fact that a slower rate of glucose consumption will permit brain glucose to more closely approach blood glucose during life. A marked increase of brain glucose is also seen in anesthesia and the extent of this increase has led others to suggest that, in addition to a decreased glucose consumption in anesthesia, there may be a primary increase of transport of glucose into brain (10,11). An increase in the extracellular fluid volume of brain in anesthesia and uremia could also produce a high brain glucose.…”

Section: Resultsmentioning

confidence: 99%

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Brain metabolism in uremic and adenosine-infused rats

Noort¹,

Eckel²,

Brine³

et al. 1968

J. Clin. Invest.

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A B S T R A C T Analyses of nucleotides and glycolytic intermediates were performed on perchlorate extracts of blood and quick-frozen brain from rats nephrectomized 48 hr previously, and from rats infused for 6 hr with adenosine or AMP. Blood nucleotides of acutely uremic rats were normal. Uremic brain showed an increase of creatine phosphate (CP), ATP, and glucose with a corresponding decrease in creatine, ADP, AMP, and lactate. Other nucleotide triphosphates were increased, but total adenine nucleotide in brain was unchanged. Uremic brain failed to use ATP or produce ADP, AMP, and lactate at normal rates when subjected to the stress of ischemic anoxia. Although levels of cation responsive ATPase in extracts of uremic brain were normal, the inhibition of glycolysis in the intact brain appeared to be due to a failure of ATP hydrolysis (a diminished ATPase activity). Adenosine infusion produced mild azotemia, marked hyperglycemia, an increase in blood ATP,-and an increase in total blood adenine nucleotide. Brain from rats infused with adenosine or AMP also had high levels of ATP, creatine phosphate, and glucose, whereas levels of ADP, AMP, and lactate were low. However these brains responded with normal use of ATP and normal production of lactate when stimulated by ischemic anoxia.

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Section: Resultscontrasting

confidence: 55%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Brain metabolism in uremic and adenosine-infused rats

Noort¹,

Eckel²,

Brine³

et al. 1968

J. Clin. Invest.

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“…The relationship of cerebral glucose and pentobarbital levels and physiological effects are summarized in table 2. It has previously been reported that pentobarbital causes an elevation of brain glucose content 17 and a decrease in body temperature. 22 The results in the present study confirm these observations, but indicate that no significant change in either parameter occurs at cerebral pentobarbital levels less than 45 fig per g. In addition, animals whose brain content of pentobarbital was less than 20 jig per g were conscious, mobile, and appeared only slightly sedated.…”

Section: Figure 2 Demonstrating the Linearity Of 2-dog Phosphorylatimentioning

confidence: 99%

“…Since the pentobarbital concentration in the cortex has been determined to be constant between 10 and 30 min after intraperitoneal injection, 16 the measurement of glucose utilization is initiated 10 min after intraperitoneal injection of sodium pentobarbital to permit the content 17 and utilization 7 of brain glucose to achieve a new steady state level. 2) Known but tracer concentrations of cerebral 2-DOG and 2-DOGP and a linear rate of 2-DOG phosphorylation must be present during the interval of measurement.…”

Section: Calculation Of the Rate Of Glucose Utilizationmentioning

confidence: 99%

Dose dependent reduction of glucose utilization by pentobarbital in rat brain.

Crane¹,

Braun²,

Cornford³

et al. 1978

Stroke

153

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Downloaded fromPENTOBARBITAL AND GLUCOSE UTILIZATION/Crane et al. 13permits the calculation of the rate of brain regional glucose utilization from individual animals, independent of measurements of blood flow and blood brain barrier transport. The additional measurement of brain pentobarbital levels by gas chromatography (GC) has enabled us to report the correlation between brain level of pentobarbital and the rate of glucose utilization. Methods Injection of Barbiturate and Radiolabeled 2-DOGWistar rats (200-250 g), of either sex, were injected intraperitoneally with 0.5 ml of Ringer's solution containing variable doses of sodium pentobarbital. After 10 min, the rats were placed in a restraining device (Gerling-Moore, Palo Alto) and their tails warmed for 30 sec in warm water. A 23 gauge needle was inserted into the dilated tail vein and ten fid of ( 3 H(G)) 2-DOG (sp. act., 10 Ci/mmole) in 0.25 ml of Ringers solution injected, followed by a 0.1 ml wash of Ringers solution. Two minutes later, 2 j*Ci of 2-(l-14 C)-DOG (sp. act., 54 mCi/mmole) in 0.25 ml of Ringers solution were injected through the same needle, followed by 0.1 ml of Ringers solution. Two minutes after the 14 C injection, the rats were killed by intense microwave irradiation.9 Cardiac blood was collected into a heparinized syringe for liquid scintillation counting. The time course of 2-DOG uptake and phosphorylation was determined by single ( 3 H) 2-DOG injections, followed by microwaving at varying times after injection. The brains were excised and stored at -20°C for subsequent analysis. Biochemical And Radiochemical AnalysisThe brains were thawed and the cerebral cortices were weighed and placed in Ten Broeck homogenizers with a measured amount of distilled water (=1.6 ml water -cortex wet wt X 0.8) and 50 #g of sodium secobarbital in 4 ml of methanol to serve as an internal standard in GC. Using a modified procedure of Bligh and Dyer, 10 the cortices were homogenized, 2 ml of chloroform were added, and the tissues were rehomogenized. The homogenates were centrifuged, the supernates saved, and the pellets rehomogenized in 7 ml of chloroform-methanol-water (1:2:0.8) and centrifuged. The supernates were combined, 5 ml of chloroform and 5 ml of water added and the aqueous and organic phases separated after centrifugation. The interfaces were washed three times with methanol-water (1:1), and the washes combined with the aqueous phases.The aqueous phases were further fractionated into neutral (containing glucose and 2-DOG) and anionic (containing 2-deoxy-D-glucose-6-phosphate (2-DOGP)) fractions by ion exchange chromatography on DEAE Sephadex A25 columns (1 ml bed volume). The neutral fractions were recovered unbound from the column, while the anionic fractions were eluted with 0.5M pyridine acetate, pH 5.0. Aliquots were removed from both fractions for simultaneous 3 H and 14 C liquid scintillation counting. The neutral fractions were dried by rotary evaporation and taken up in a 0.1M Tris-HCl (buffered to pH 7.5) and 0.02% sodium azide solution f...

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Brain Metabolism in Experimental Uremia

Noort¹

1970

Arch Intern Med

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The Glucose Content of Brain in Anaesthesia*

Cited by 127 publications

References 8 publications

Brain metabolism in uremic and adenosine-infused rats

Brain metabolism in uremic and adenosine-infused rats

Dose dependent reduction of glucose utilization by pentobarbital in rat brain.

Brain Metabolism in Experimental Uremia

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