Movements of radioactive carbon dioxide within the animal body during oxidation of <sup>14</sup>C‐labelled substances

Coxon, R. V.; Robinson, Robert J.

doi:10.1113/jphysiol.1959.sp006258

Cited by 20 publications

(5 citation statements)

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“…The latter type of non-homogeneity has been postulated by Renkin (1959) to account for his findings with regard to the penetration of radioactive potassium into muscle. Moreover, in practice, multiple rather than single exponential terms are commonplace in the equations describing the time course of mixing of tracer substances introduced into the blood stream with preexisting body pools (Robertson, 1956); and in the case of labelled carbon dioxide there is some evidence that the rate of exchange of molecules between tissue and blood can be correlated with the ratio of the size of the tissue pool to the regional blood flow (Coxon & Robinson, 1959). It is important to recall in this connexion that Conway & Fitzgerald (1942) inferred from a consideration of data obtained under different experimental conditions from ours the existence of four compartments in the water of the c.N.s.…”

Section: Resultsmentioning

confidence: 99%

The penetration of urea into the central nervous system at high blood levels

Bradbury¹,

Coxon²

1962

The Journal of Physiology

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Evidence has been presented during the past few years that intravenous administration of hypertonic solutions of urea has the effect of reducing intracranial pressure and inducing shrinkage of the brain in patients undergoing neurosurgical treatment (Javid & Settlage, 1956;Stubbs & Pennybacker, 1960). In considering mechanisms by which such effects might arise one possibility which comes to mind is that the urea may act in a similar manner to other solutes, such as sodium chloride, which have similar effects when injected in hypertonic solution (Weed & McKibben, 1919) and which are believed to bring about withdrawal of water from the cerebral tissue by virtue of the increased osmotic pressure of the blood plasma which results from their presence in it. However, an obvious difficulty about accepting such an explanation in the case of urea is the fact that this substance is generally held to distribute itself freely throughout the whole of the intracellular as well as the extracellular water of the human body (McCance & Widdowson, 1951) and, in particular, it appears not to behave as an osmotically active solute in relation to the membrane of the receptor organs responsible for controlling the output of antidiuretic hormone which are believed to lie in the hypothalamic area of the brain (Verney, 1954).The experiments reported in this paper were undertaken in order to determine directly the extent to which intravenously injected urea would penetrate the water of central nervous structures, and hence to study its ability to promote the transfer of water from the brain cells under a simple osmotic gradient. The opportunity was also taken to collect data on changes in water and electrolyte content of brains from animals exposed to constantly elevated concentrations of urea in their blood for periods of several hours. The majority of the experiments were done on cats but isolated observations were also made on a rabbit and a dog.27-2 424 M. W. B. BRADBURY AND R. V. COXON METHODS Preparation of animal. Seventeen adult cats, fourteen males and three females, weighing between 2-0 and 4-8 kg, were used for the main investigation. All animals were deprived of food for 16 hr and were initially anaesthetized with intraperitoneal sodium pentobarbitone 49 mg/kg body wt., supplemented by further small doses of the same drug given intravenously as required. Plastic tubing inserted through the left femoral vein into the inferior vena cava was used for infusions, and the right femoral artery was cannulated to provide for the withdrawal of blood samples. The urethra was then catheterized and the abdomen opened in order that the bladder might be compressed to facilitate complete emptying. For the priming dose 'Urevert' (Baxter Laboratories Ltd.), which is a sterile solution containing 30 g/100 g urea and 6-5 % invert sugar, was injected over 5-10 min into the inferior vena cava, 4-0 ml. being given/kg body wt. of cat. Further urea was administered as a 3 or 6 % solution with 5 % glucose by means of an electrically driven syringe; con...

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Section: Resultsmentioning

confidence: 99%

The penetration of urea into the central nervous system at high blood levels

Bradbury¹,

Coxon²

1962

The Journal of Physiology

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“…We cannot say in which tissues this oxidation takes place. It is unlikely to be in limb muscle (Andres, Cader & Zierler, 1956;Coxon & Robinson, 1959b).…”

Section: Maureen Ashby and Othersmentioning

confidence: 99%

A quantitative study of carbohydrate metabolism in the normal and injured rat.

Ashby¹,

Heath²,

Stoner³

1965

The Journal of Physiology

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This work arose out of study of the effect of severe injury on the metabolism of the rat. Its aim was to determine how carbohydrate metabolism differed in injured and normal rats. From the review of Levenson, Einheber & Malm (1961) it is clear that although the effect of injury on metabolism has been studied for a long time there is still much to be learnt. In the past, studies have been, for the most part, confined to determinations of the concentrations of metabolites in tissues. In the case of carbohydrate metabolism this is not enough. Besides concentrations of metabolites the rates of metabolism along the various pathways, glycolytic, gluconeogenic and oxidative, are also required. These rates can only be studied in whole animals by using tracers.We have, therefore, injected control and injured rats intravenously with U-14C-glucose, U-14C-fructose and 1_14C_, 2_14C-and 3-14C-pyruvates. We have followed the disappearance of 14C-glucose and 14C-fructose from the blood and the appearance and subsequent disappearance of 14C-glucose after the injection of 14C-fructose and the labelled pyruvates. The excretion of 14CO2 formed by the oxidation of these compounds in vivo was also followed. In this way the glycolytic and gluconeogenic pathways were spanned by 14C-glucose and 14C-pyruvate while 14C-fructose could be expected to provide information on processes in the middle, as its label enters them mainly as triose phosphate (Hers & Kusaka, 1953;Leuthardt, Testa & Wolf, 1953).Results obtained from experiments of this type show only the combined effects of distribution and metabolism. To separate these two effects one must find a method of interpretation which allows for their interaction. Unless this is done even qualitative conclusions may be wrong and it is quite impossible to make quantitative estimates. The only technique which offers some hope of separating distributive and metabolic processes is compartmental analysis (Sheppard, 1962). Theoretical models which reproduce the most important features of these processes are set up and analysed mathematically. No model can take account of all the processes, 13 Physiol. 179

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“…Nevertheless, it is probable that equilibration within the body bicarbonate pool had not been reached (20)(21)(22)(23); if so, the amount of circulating glucose converted to C02 during these experiments is underestimated.…”

Section: Glucose Turnover and Oxidation By The Primed Infusion Technicmentioning

confidence: 99%

Glucose Turnover and Disposal in Maturity-Onset Diabetes

Bowen¹,

Moorhouse²

1973

J. Clin. Invest.

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A B S T R A C T The glucose turnover rate in maturityonset diabetes in man has been variously reported as increased, normal, and decreased. The present experiments suggest that these discrepancies may have been due to methodology, and to nonrecognition of a circadian cycle in the glucose turnover rate that is present in health, and marked in diabetes.During the early morning hours the glucose turnover rate in maturity-onset diabetes is increased in proportion to the fasting blood glucose level. It may reach three to four times the rate found in health. During the evening hours the increments are about one-half as great.The glucose outflow rate constant, k, lower in diabetes than in health, is also lower in both groups in the evening than in the morning.An analysis of the relative contributions of glucose overproduction and underutilization to the development of hyperglycemia in maturity-onset diabetes indicates that overproduction is the greater factor. The relative role of underutilization appears to increase as the fasting blood glucose level increases.The circulating glucose oxidation rate in maturityonset diabetes is only slightly lower than in health, but the fraction oxidized is markedly lower, and only a small fraction is excreted.The principal conclusion is that in maturity-onset diabetes there is a hypertrophied flux of endogenous glucose, most of which is neither oxidized nor excreted. The precursors and the qualitative and quantitative metabolic fates of this excess glucose are unknown.

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Movements of radioactive carbon dioxide within the animal body during oxidation of ¹⁴C‐labelled substances

Cited by 20 publications

References 19 publications

The penetration of urea into the central nervous system at high blood levels

The penetration of urea into the central nervous system at high blood levels

A quantitative study of carbohydrate metabolism in the normal and injured rat.

Glucose Turnover and Disposal in Maturity-Onset Diabetes

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Movements of radioactive carbon dioxide within the animal body during oxidation of 14C‐labelled substances

Cited by 20 publications

References 19 publications

The penetration of urea into the central nervous system at high blood levels

The penetration of urea into the central nervous system at high blood levels

A quantitative study of carbohydrate metabolism in the normal and injured rat.

Glucose Turnover and Disposal in Maturity-Onset Diabetes

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Product

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Movements of radioactive carbon dioxide within the animal body during oxidation of ¹⁴C‐labelled substances