Membrane permeability equations and their solutions for red cells

1977 ◽  
Vol 34 (1) ◽  
pp. 103-144 ◽  
Author(s):  
Jerome H. Milgram ◽  
A. K. Solomon
Keyword(s):  
Membrane Permeability ◽  
Red Cells

scholarly journals Red Cell Membrane Permeability Deduced from Bulk Diffusion Coefficients

1974 ◽  
Vol 64 (6) ◽  
pp. 706-729 ◽  
Author(s):  
W. R. Redwood ◽  
E. Rall ◽  
W. Perl
Keyword(s):  
Cell Membrane ◽  
Membrane Permeability ◽  
Diffusion Coefficients ◽  
Bulk Diffusion ◽  
Red Cells ◽  
Cell Membrane Permeability ◽  
Red Cell ◽  
Cell Column ◽  
Red Cell Membrane ◽  
One Dimensional

The permeability coefficients of dog red cell membrane to tritiated water and to a series of[14C]amides have been deduced from bulk diffusion measurements through a "tissue" composed of packed red cells. Red cells were packed by centrifugation inside polyethylene tubing. The red cell column was pulsed at one end with radiolabeled solute and diffusion was allowed to proceed for several hours. The distribution of radioactivity along the red cell column was measured by sequential slicing and counting, and the diffusion coefficient was determined by a simple plotting technique, assuming a one-dimensional diffusional model. In order to derive the red cell membrane permeability coefficient from the bulk diffusion coefficient, the red cells were assumed to be packed in a regular manner approximating closely spaced parallelopipeds. The local steady-state diffusional flux was idealized as a one-dimensional intracellular pathway in parallel with a one-dimensional extracellular pathway with solute exchange occurring within the series pathway and between the pathways. The diffusion coefficients in the intracellular and extracellular pathways were estimated from bulk diffusion measurements through concentrated hemoglobin solutions and plasma, respectively; while the volume of the extracellular pathway was determined using radiolabeled sucrose. The membrane permeability coefficients were in satisfactory agreement with the data of Sha'afi, R. I., C. M. Gary-Bobo, and A. K. Solomon (1971. J. Gen. Physiol. 58:238) obtained by a rapid-reaction technique. The method is simple and particularly well suited for rapidly permeating solutes.

scholarly journals Analytical Review: Leaky Red Cells

Blood ◽  
1965 ◽  
Vol 26 (3) ◽  
pp. 367-382 ◽  
Author(s):  
JAMES H. JANDL
Keyword(s):  
Membrane Permeability ◽  
Active Transport ◽  
Hereditary Spherocytosis ◽  
Metabolic Stress ◽  
Glucose Deprivation ◽  
Red Cells ◽  
Osmotic Swelling ◽  
Permeability Changes ◽  
Metabolic Conditions ◽  
Analytical Review

Abstract The normal survival of red cells requires maintained regulation of cell size and shape. This regulation is to a large extent dependent upon membrane permeability and the active transport of cations. Agents such as C' that affect permeability markedly by creating large holes in the membrane lead to rapid cell death. Most hemolytic disorders thus far studied involve lesser increases in membrane permeability and hemolysis occurs more gradually by the sequence of colloid osmotic swelling, loss of cell surface, and spherocytosis. With very mild permeability changes, as in hereditary spherocytosis, the cell may compensate for an increased leak-rate for cations by increased active transport. This compensation requires increased glycolysis and optimal metabolic conditions, however, and the cell rapidly decompensates during glucose deprivation or metabolic stress. The interaction between reticuloendothelial tissues and red cells provides such a stress for leaky cells and hastens their destruction.

The membrane permeability of nonelectrolytes and carbohydrate metabolism of Amazon fish red cells

1978 ◽  
Vol 56 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Hyun Dju Kim ◽  
R. E. Isaacks
Keyword(s):  
Membrane Permeability ◽  
Carbohydrate Metabolism ◽  
Diffusion Mechanism ◽  
Red Cells ◽  
Facilitated Diffusion ◽  
Metabolic Substrates ◽  
Urea Permeability ◽  
Arapaima Gigas ◽  
Electric Eel ◽  
Order Of Magnitude

The membrane permeability to nonelectrolytes and carbohydrate metabolism were examined in red cells obtained from the Amazon fishes including the electric eel (Electrophorus electrocus), the arawana (Osteoglossum bicirrhosum), the pirarucu (Arapaima gigas), the lungfish (Lepidosireti paradoxa), and the armored catfish (Pterygoplichthys). Glucose permeability was fastest in the electric eel, followed by the lungfish. The red cells of the arawana were only slightly permeable to glucose. Both the armored catfish and the pirarucu red cells were found to be totally impermeable to glucose. There was no evidence for the presence of the facilitated diffusion mechanism for glucose transport in any of these fish red cells. In sharp contrast with glucose, red cells of all five species were quite permeable to ribose and urea. Urea permeability of red cells decreased in order of magnitude with the lungfish > the electric eel > the arawana > the armored catfish [Formula: see text] the pirarucu. The urea permeability of the lungfish was inhibited in the presence of phloretin.Of the two metabolic substrates, glucose but not ribose was metabolized to lactate with a concomitant contribution to ATP maintenance by the lungfish red cells. Even though the glucose-impervious pirarucu cells could not utilize glucose, ribose was readily metabolized by the pirarucu cells.

scholarly journals ELECTRIC IMPEDANCE OF INJURED AND SENSITIZED RED BLOOD CORPUSCLES

1936 ◽  
Vol 20 (1) ◽  
pp. 105-109 ◽  
Author(s):  
Howard J. Curtis
Keyword(s):  
Electrical Properties ◽  
Membrane Permeability ◽  
Tannic Acid ◽  
Silicic Acid ◽  
Red Cells ◽  
Frequency Variation ◽  
Electric Impedance ◽  
Low Frequencies ◽  
Membrane Changes

On the basis of previous work on the electrical properties of hemolyzed red cells, it might be supposed that the variation of the capacity with frequency at low frequencies is an indication of membrane permeability. To test this, rabbit red cells were subjected to treatment with lecithin, tannic acid, glucose, saponin, amboceptor, and colloidal silicic acid, each in sub-lytic doses. No change in any of the electrical properties of any of the suspensions could be detected. The result may mean that the form of the frequency variation is an extremely insensitive measure of permeability and other membrane changes, and capable only of disclosing the very great changes associated with hemolysis, or it may mean that the change in the frequency variation at low frequencies has nothing to do with permeability.

scholarly journals The Reponse of Duck Erythrocytes to Norepinephrine and an Elevated Extracellular Potassium

1973 ◽  
Vol 61 (4) ◽  
pp. 509-527 ◽  
Author(s):  
Floyd M. Kregenow
Keyword(s):  
Membrane Permeability ◽  
Cell Size ◽  
Monovalent Cation ◽  
Red Cells ◽  
Extracellular Potassium ◽  
Solute Content ◽  
Cation Content ◽  
Controlling Mechanism ◽  
Cation Pump ◽  
Original Size

This paper presents evidence that duck erythrocytes regulate their size in isotonic media by utilizing a previously reported "volume-controlling mechanism." Two different experimental situations are examined. In the first, cells enlarge in a solution containing norepinephrine and an elevated [K]o; and in the second, enlarged cells shrink to their original size if the norepinephrine and excess potassium are removed. As the erythrocytes enlarge, K, Cl, and H2O accumulate. Shrinkage, in contrast, is accompanied by the controlled loss of K, Cl, and H2O. These changes and the associated changes in membrane permeability resemble those reported previously when duck erythrocytes incubate in anisotonic media. There cells, after first shrinking or swelling, utilize a "volume-controlling mechanism" to reestablish their original size. The mechanism regulates cell size by adjusting the total number of osmotically active intracellular particles. The present studies indicate duck red cells use this mechanism to readjust their total monovalent cation content and thus their solute content in isotonic media as well. In addition, evidence is presented which indicates that the "volume-controlling mechanism" and ouabain-inhibitable cation pump differ functionally.

scholarly journals Organotin-mediated exchange diffusion of anions in human red cells.

1979 ◽  
Vol 73 (6) ◽  
pp. 765-788 ◽  
Author(s):  
J O Wieth ◽  
M T Tosteson
Keyword(s):  
Membrane Permeability ◽  
Anion Exchange ◽  
Ion Pairs ◽  
Chloride Ion ◽  
Chloride Ions ◽  
Red Cells ◽  
Exchange Diffusion ◽  
Tributyltin Chloride ◽  
Chloride Exchange ◽  
Red Cell Membranes

Organotin cations (R3Sn+) form electrically neutral ion pairs with monovalent anions. It is demonstrated that the tin derivatives induce exchange diffusion of chloride in red cells and resealed ghosts, without any detectable increase of membrane permeability to net movements of chloride ions. The obligatory anion exchange is believed to be due to the permeation of electroneural ion pairs, whereas the organic cation (R3Sn+) has an extremely low membrane permeability. Exchange fluxes of chloride increased with the lipophilicity of the substituting group (R3). At the same molar concentration of organotin, the relative potencies of the tin derivatives as anion carriers (with trimethyltin as a reference) were: methyl 1, ethyl 30, propyl = phenyl 1,00, and butyl 10,000. Tributyltin-mediated anion exchange was studied in detail. The organotin-induced anion transport increased through the sequence: F- less than Cl- less than Br- less than I- = SCN- less than OH-. Partitioning of tributyltin into red cell membranes was greater in iodide than in chloride media (partition coefficients 6.6 and 1.7 x 10(-3) cm, respectively). Bicarbonate, fluoride, nitrate, phosphate, and sulphate did not exchange with chloride in the presence of tributyltin. Chloride exchange fluxes increased linearly with tributylin concentrations up to 10(-5) M, and with chloride concentrations up to at least 0.9 M. The apparent turnover number for tributyltin-mediated chloride exchange increased from 15 to 1,350 s-1 between 0 and 38 degrees C. These figures are minimum turnover numbers, because it is not known what fraction of the organotin in the membrane exists as chloride ion pairs.

Initial Polymerization Sites Indicated During Mitochondrial Oxidation of Diaminobenzidine after Toluene Treatment

1977 ◽  
Vol 35 ◽  
pp. 408-409
Author(s):  
W. A. Shannon ◽  
M. A. Matlib
Keyword(s):  
Membrane Permeability ◽  
Cytochrome Oxidase ◽  
Rat Liver ◽  
Precise Definition ◽  
Cytochemical Localization ◽  
Oxidative Reaction ◽  
Mitochondrial Oxidation ◽  
Definition Of ◽  
Exogenous Substrates

Numerous studies have dealt with the cytochemical localization of cytochrome oxidase via cytochrome c. More recent studies have dealt with indicating initial foci of this reaction by altering incubation pH (1) or postosmication procedure (2,3). The following study is an attempt to locate such foci by altering membrane permeability. It is thought that such alterations within the limits of maintaining morphological integrity of the membranes will ease the entry of exogenous substrates resulting in a much quicker oxidation and subsequently a more precise definition of the oxidative reaction.The diaminobenzidine (DAB) method of Seligman et al. (4) was used. Minced pieces of rat liver were incubated for 1 hr following toluene treatment (5,6). Experimental variations consisted of incubating fixed or unfixed tissues treated with toluene and unfixed tissues treated with toluene and subsequently fixed.

Sarcolemmal permeability changes during early myocardial anoxia

1978 ◽  
Vol 36 (2) ◽  
pp. 642-643
Author(s):  
M. Ashraf ◽  
L. Landa ◽  
L. Nimmo ◽  
C. M. Bloor
Keyword(s):  
Cell Membrane ◽  
Membrane Permeability ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Cell Membrane Permeability ◽  
Enzyme Release ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sarcolemmal Permeability ◽  
Membrane Changes

Following coronary artery occlusion, the myocardial cells lose intracellular enzymes that appear in the serum 3 hrs later. By this time the cells in the ischemic zone have already undergone irreversible changes, and the cell membrane permeability is variably altered in the ischemic cells. At certain stages or intervals the cell membrane changes, allowing release of cytoplasmic enzymes. To correlate the changes in cell membrane permeability with the enzyme release, we used colloidal lanthanum (La+++) as a histological permeability marker in the isolated perfused hearts. The hearts removed from sprague-Dawley rats were perfused with standard Krebs-Henseleit medium gassed with 95% O2 + 5% CO2. The hypoxic medium contained mannitol instead of dextrose and was bubbled with 95% N2 + 5% CO2. The final osmolarity of the medium was 295 M osmol, pH 7. 4.

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