STUDIES IN THE METABOLISM OF SODIUM r-LACTATE. I. RESPONSE OF NORMAL HUMAN SUBJECTS TO THE INTRAVENOUS INJECTION OF SODIUM r-LACTATE

Hartmann, Alexis F.; Senn, Milton J. E.

doi:10.1172/jci100414

Cited by 88 publications

(32 citation statements)

References 6 publications

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“…Previous studies have been made of the effects of alkalinizing sodium solutions. Palmer and Van Slyke (2) and later Hartmann and Senn (3) found that the rise in serum bicarbonate was such that the dose of alkali was apparently distributed through a volume equal to two-thirds of the body weight, a fraction which they believed represented the total body water. Since both bicarbonate ions (4,5) and the major portion of sodium ions are not freely diffusible across the cell membrane, some explanation must be sought for the discrepancy between the value stated above and the now commonly accepted 1 Laboratory facilities were aided by grants from the National Heart Institute, U.S.P.H.S., the C. Mahlon Kline Fund of the Department of Medicine, and the Committee on the Advancement of Research of the University of Pennsylvania.…”

mentioning

confidence: 99%

Intracellular Cation Exchanges in Acidosis Due to Renal Insufficiency. Effects of Alkali Therapy 1

Elkinton¹,

Squires²,

Singer³

1951

J. Clin. Invest.

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Disturbances in the exchanges of certain intracellular electrolytes which occur in patients with metabolic alkalosis, have been described in the previous paper (1). Clues to the direction and magnitude of these disturbances were obtained by calculating from balance measurements the alterations in body fluids produced by replacement therapy. In the present communication the results are presented of a similar study in patients with metabolic acidosis due to renal insufficiency.Since this study involved the administration of hypertonic solutions of sodium bicarbonate or sodium lactate, it seemed advisable to reassess all of the factors, including those of intracellular transfers, which determine the quantitative effect of such replacement therapy on the total fluid and acid-base equilibrium of these patients. Previous studies have been made of the effects of alkalinizing sodium solutions. Palmer and Van Slyke (2) and later Hartmann and Senn (3) found that the rise in serum bicarbonate was such that the dose of alkali was apparently distributed through a volume equal to two-thirds of the body weight, a fraction which they believed represented the total body water. Since both bicarbonate ions (4, 5) and the major portion of sodium ions are not freely diffusible across the cell membrane, some explanation must be sought for the discrepancy between the value stated above and the now commonly accepted

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mentioning

confidence: 99%

Intracellular Cation Exchanges in Acidosis Due to Renal Insufficiency. Effects of Alkali Therapy 1

Elkinton¹,

Squires²,

Singer³

1951

J. Clin. Invest.

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“…Moreover the effect of sodium bicarbonate treatment often produced too rapid correction of the acidosis and indeed could produce a profound alkalosis. An alternative to sodium bicarbonate was needed [4].…”

Section: Discussionmentioning

confidence: 99%

“…1) as indicated by the unidirectional arrows. In normal healthy adults a transient increase in blood glucose is registered [4], provoking an appropriate insulin response. Metabolism by oxidation of the lactate (about 30%) is ........................................................................................................................................................................................................................................... …”

Section: Discussionmentioning

confidence: 99%

“…Thus a steady stream of alkalinising agent is generated, reducing acidosis in a controlled fashion. If there is no acidosis to correct then the bicarbonate is usually excreted promptly by the kidneys and the mild alkalosis is transient [4]. However some critically ill patients are obligate excretors of acidic urine and the additional bicarbonate load generated from the lactate cannot be excreted, rendering the patient alkalotic and enhancing renal potassium loss [5].…”

Section: S a White And D R Goldhillmentioning

confidence: 99%

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Is Hartmann's the solution?

White

Goldhill

1997

Anaesthesia

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SummaryAs Hartmann's solution is commonly used by anaesthetists, we surveyed a group of Part III FRCA candidates to establish their knowledge of its constituents and the purpose and metabolism of the lactate in solution. Of the 82 candidates surveyed only three (4%) accurately recorded the electrolytes and their concentrations in Hartmann's solution. Lactate was stated to be a source of bicarbonate by 52 (63%) and a source of glucose by 17 (21%). The descriptions of lactate metabolism were largely imprecise, none was complete and 24 (29%) of candidates offered no explanation. The constituents of Hartmann's solution and their concentrations are designed to match those of plasma, reducing ion and fluid shifts postinfusion. The lactate in Hartmann's solution is metabolised by both oxidation and gluconeogenesis, predominantly in the liver, and bicarbonate is generated by both processes over 1-2 h. Hartmann's solution is often regarded as the anaestheticpanacea of fluid resuscitation. This crystalloid formulation is routinely employed as the rehydration and maintenance solution of choice in the operating theatre. In discussion with colleagues it became apparent that knowledge regarding the concentration of the constituent ions and the metabolism of the lactate content varied widely. We therefore decided to assess the level of knowledge about Hartmann's solution amongst the wider anaesthetic community. MethodsWe obtained permission from The Royal College of Anaesthetists to survey candidates attending the Part III FRCA College course in February 1996. At the end of an afternoon lecture session, those present were asked to complete a voluntary and confidential questionnaire. The candidates were given no time limit for completing the task, but were instructed not to confer with each other, nor to refer to texts. The questionnaire (see Appendix 1) asked for the following information: 1 the constituents and their concentrations in 1 litre of 0.9% sodium chloride; 2 the constituents and their concentrations in 1 litre of Hartmann's solution; 3 the purpose of the lactate in Hartmann's solution; 4 the metabolism of the lactate in Hartmann's solution.In addition to the survey, we also reviewed the anaesthetic textbooks present in the anaesthetic library of The Royal London Hospital to establish the availability of 'source information' under the following headings: 1 Hartmann's solution -constituents, metabolism; 2 Ringer's lactate solution -constituents, metabolism; 3 lactate metabolism.

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“…The dose of molar solution of sodium lactate administered in each case was calculated, according to the formula given by Hartmann and Senn (16), to raise the alkali reserve of the body fluids by 20 volumes per cent. The solution was diluted with 2 to 3 volumes of water and injected into a leg vein.…”

Section: Methodsmentioning

confidence: 99%

The Acidosis of Guanidine Intoxication 1

Minot

Dodd²,

Saunders³

1934

J. Clin. Invest.

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Recent reports (1) (2) (3) (4) (5) which implicate guanidine intoxication as a complicating factor in some instances of acute liver injury, of eclampsia, and of alimentary intoxication in infants, make it desirable to know in greater detail the effect of guanidine on various biological processes. Only in this way can we know in what manner increased guanidine may modify the clinical picture in a given disease and may influence the response of the patient to treatment of his symptoms. Since acidosis must often be treated in the presence of hyperguanidinemia, it is of interest to study the effect of guanidine intoxication on the acid base equilibrium.Various observers have mentioned breathing of the " air hunger " type in guanidine poisoning. Watanabe (6) reported a decrease in pH and CO2 of the blood and an increased output of ammonia in the urine of experimental animals poisoned with guanidine. His results were disputed by Gy6rgy and Vollmer (7) who argued that a condition of alkalosis rather than acidosis must be produced since the hyperirritability caused by guanidine can be relieved by the administration of acid. These authors, however, presented no studies of acid base equilibrium to substantiate their claims. We already have considerable evidence that one feature of the intoxication is a serious disturbance of lactic acid metabolism. In an investigation of the hypoglycemia induced by guanidine and by its derivative synthalin, Staub (8) showed that lactic acid accumulates in the tissues and body fluids and is excreted in the urine. He attributes this accumulation to the inability of tissues poisoned with guanidine to oxidize and resynthesize lactic acid to its precursors in a normal manner. Gradually more and more of the carbohydrate reserve is transformed to lactic acid until a severe hypoglycemia results. Minot (9) confirmed these observations both in experimental guanidine poisoning and in the intoxication which occurs when hyperguanidinemia is a result of acute extensive necrosis of the liver. Although no acid base studies were reported in connection with either of these investigations one would expect that, as lactic acid accumulates and is neutralized, there would be a progressive depletion of the alkali reserve.

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STUDIES IN THE METABOLISM OF SODIUM r-LACTATE. I. RESPONSE OF NORMAL HUMAN SUBJECTS TO THE INTRAVENOUS INJECTION OF SODIUM r-LACTATE

Cited by 88 publications

References 6 publications

Intracellular Cation Exchanges in Acidosis Due to Renal Insufficiency. Effects of Alkali Therapy 1

Intracellular Cation Exchanges in Acidosis Due to Renal Insufficiency. Effects of Alkali Therapy 1

Is Hartmann's the solution?

The Acidosis of Guanidine Intoxication 1

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