Factors controlling the electrolyte and water distribution in the blood

Slyke, Donald D. Van; Wu, Ho‐Ting; McLean, Franklin C.

doi:10.3181/00379727-20-106

Cited by 66 publications

(98 citation statements)

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“…His results were confirmed by Collip (16) who explained the high freezing point depression of excised tissue by assuming the activation of osmotically inert particles in the tissue after removal. Along other lines, the observation of tissue swelling in isotonic solutions has been made repeatedly by many early workers [7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Swelling was usually accounted for by the implicit assumption of cellular isotonicity initially with the subsequent production of osmotically active particles derived from the catabolic reactions of glycogen or proteins.…”

Section: Introductionmentioning

confidence: 99%

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The Freezing Point Depression of Mammalian Tissues in Relation to the Question of Osmotic Activity of Cell Fluid

Brodsky

Appelboom

Dennis

et al. 1956

The Journal of General Physiology

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The freezing point depression of freshly excised frozen tissues, pulverized in a hydraulic press or in a mortar, is greater than that of plasma. Even at 0°C. the freezing point depression of such homogenates increases significantly with time. Dilution data indicate that such freezing point data are valid. The presence of intact cells has been shown in smears of tissues pulverized in a mortar, but not in smears of those crushed in a hydraulic press. The osmolarity of various diluent solutions affects the calculated osmotic activity of tissue homogenates presumably because of delayed diffusion between the diluent and cell fluid. With a hypertonic NaCl diluent, spuriously low values of tissue osmotic activity are found from calculations assuming instantaneous mixing between homogenates and diluents. The limitations of data from cryoscopic experiments and from tissue-swelling experiments are discussed in relation to the basic question of whether or not cell fluid is isotonic to extracellular fluid.

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Section: Introductionmentioning

confidence: 99%

“…Moreover, erythrocytes behave as nearly perfect osrnorneters when suspended in solutions of varying osrnolarity (7); (b) the estimated sum of the rnolal concentrations of solutes in erythrocytes and muscle (8)(9)(10)(11); (c) changes in serum osrnolarity after injection of hypertonic solutions into intact animals (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

The Freezing Point Depression of Mammalian Tissues in Relation to the Question of Osmotic Activity of Cell Fluid

Brodsky

Appelboom

Dennis

et al. 1956

The Journal of General Physiology

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“…According to VAN SLYKE et al (1923), the change in buffer base in the RBC is expressed by a product of a buffer value of hemoglobin, j9,, (mmol/(l RBC.pH0)) and 4pH0. For instance, when dehydration of HC03-occurs, the buffer base increases parallel to the change in Pco2 and pH0.…”

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confidence: 99%

Change in PCO2 in red cell suspension following bicarbonate shift.

Shimouchi¹,

Mochizuki²,

Niizeki³

1984

Jpn.J.Physiol

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To reveal the C02 diffusion process into and out of the red blood cell (RBC), changes in Pco2 following the HC03-shift were examined. The RBC suspension was mixed at 37°C with saline solution having different HC03-concentrations. In proportion to the intracellular HC03-change caused by the HC03-shift, the P02 change was increased. The rate of change increased as the hematocrit and the initial intracellular HC03-content decreased. For calculating the above Pco2 change, a theoretical equation was derived from the HendersonHasselbalch equation and the relation between both the changes in buffer base and intracellular pH. The calculated Pco2 change coincided well with the measured value, suggesting the validity of the theoretical equations.Key Words: HC03-shift, Pco2 change, Henderson-Hasselbalch equation, intracellular pH, buffer value.For clarifying C02 exchange rate in vivo, it is necessary to determine the diffusion rates of C02 and HC03-into and out of the red blood cell (RBC) as well as their interactions with oxygen. For estimating the above diffusion rates a simulation method using solutions of the diffusion equations for C02 and HC03-may be the most suitable at the present time. To solve the equations numerically, in turn, such parameters as the diffusion coefficients and the permeabilities of C02 and HC03-across the RBC membrane are indispensable. Recently, NIIZEKI et al. (1984) measured the rate of HC03-shift in the RBC in which carbonic anhydrase was not inhibited. They ascertained that the Pco2 in the RBC was increased due to HC03-influx, causing outward C02 diffusion, and the outflow of HC03-caused a decrease in intracellular Pco2 and subsequently the inward C02 diffusion. In general, the HC03-shift occurs whenever C02 molecules diffuse into or out of the RBC. Therefore, the phenomenon that the HC03-shift causes the secondary C02 diffusion is very important in obtaining the theoretical equations for the C02 and HC03-diffusions.

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“…Tonometers of 300 cc. capacity were filled with the desired CO2 and 02 mixtures by the manometer method outlined by Van Slyke, Wu and McLean (7). Five cubic centimeters of blood were introduced into each tonometer.…”

Section: Methodsmentioning

confidence: 99%

Oxyhemoglobin dissociation curves of whole blood in anemia

1927

American Heart Journal

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Although the oxy-hemoglobin dissociation curves of normal whole blood have been extensively studied for many years (1, 2, 3), there has been relatively little investigation of these curves in the blood of abnormal subjects.Meakins, Dautrebande and Fetter (4), in their work on circulatory stasis in 1923, published some oxygen dissociation curves of patients with cardiac decompensation, showing that at or near 40 mm. CO2 tension, these curves did not deviate appreciably from those of normal blood. Stadie and Martin (5), investigating carbon monoxide hemoglobin and oxy-hemoglobin relations, included one oxygen dissociation curve of a patient with pernicious anemia. This was at 40 mm. C02 tension, and was an apparently normal curve. Odaira (6) stated that in severe anemia the oxygen curves were lowered, but did not state at what CO2 tension or serum pH these curves were determined.The present investigation represents a study of the oxy-hemoglobin dissociation curves of the whole blood of several subjects with anemia from various causes, and of one with advanced polycythemia vera.It comprises the following: (a) at serum pH (or pH.) 7.44 (Coi tension approximately 40 mm.), points on the 02 dissociation curves of five primary anemias, two secondary anemias, and one polycythemia vera; (b) at pH. 7.64 (CO2 tension approximately 20 mm.), points on the curves of three primary and two secondary anemias; (c) at pH3 7.24 (CO2-tension approximately 80 .), points on the curves of one. primary and on' secondary anemia. A control curve of the blood of one of us was also done at each of these CO2 tension:105

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Factors controlling the electrolyte and water distribution in the blood

Cited by 66 publications

References 0 publications

The Freezing Point Depression of Mammalian Tissues in Relation to the Question of Osmotic Activity of Cell Fluid

The Freezing Point Depression of Mammalian Tissues in Relation to the Question of Osmotic Activity of Cell Fluid

Change in PCO2 in red cell suspension following bicarbonate shift.

Oxyhemoglobin dissociation curves of whole blood in anemia

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