scholarly journals RATE OF POTASSIUM EXCHANGE OF THE HUMAN ERYTHROCYTE

1950 ◽  
Vol 33 (6) ◽  
pp. 691-702 ◽  
Author(s):  
John W. Raker ◽  
Isaac M. Taylor ◽  
John M. Weller ◽  
A. Baird Hastings
Keyword(s):  
Exchange Rate ◽  
Temperature Coefficient ◽  
Human Erythrocyte ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Red Cells ◽  
Essentially Normal ◽  
Time Required ◽  
Potassium Exchange

1. The exchange of potassium by the human erythrocyte has been studied in vitro using radioactive potassium. 2. An incubation technique which maintains erythrocytes in an essentially normal state for over 48 hours was employed. 3. Exchange of radioactive potassium between the red cells and the extracellular fluid was regular and progressive, the specific activities of the intra- and extracellular fluids reaching equal values. This indicates that all the erythrocyte potassium is exchangeable and is exchanging at the same rate. 4. From these data, it was calculated that at 37°C., 1.6 per cent of the erythrocyte potassium exchanges per hour, corresponding to an exchange of 1.5 mM of potassium per liter of red cells per hour. The time required for the exchange of 50 per cent of the red cell potassium is calculated to be 43 hours. 5. The temperature coefficient (Q10) of the potassium exchange rate is 2.2. This is the same as the temperature coefficient of the rate of utilization of glucose by the human erythrocyte. 6. Varying the percentage of red cells, plasma potassium concentration, initial glucose level, and pH between 7.0 and 7.7 had no effect on the potassium exchange rate.

Arterial Plasma Potassium Measured Continuously during Exercise in Man

1984 ◽  
Vol 67 (4) ◽  
pp. 427-431 ◽  
Author(s):  
R. A. F. Linton ◽  
M. Lim ◽  
C. B. Wolff ◽  
P. Wilmshurst ◽  
D. M. Band
Keyword(s):  
Transmembrane Potential ◽  
Venous Blood ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Receptor Sensitivity ◽  
Blood Samples ◽  
Hepatic Venous Blood ◽  
Arterial Plasma

1. Five continuous records of arterial plasma potassium were obtained from three normal subjects during brief periods (5–7 min) of exercise (100 W). 2. In two of these subjects hepatic venous blood samples were withdrawn at 0.5–1.0 min intervals and analysed in vitro for plasma potassium. 3. Arterial plasma potassium rose rapidly at the start of exercise from 3.8 ± 0.3 mmol/l (mean ± sd) to plateau levels of 5.4 ± 0.1 mmol/l. 4. One of the above subjects and a further subject were studied after β-blockade with propranolol. This resulted in an exaggerated rise in arterial plasma potassium during exercise. 5. Hepatic venous potassium measurements indicated that the liver probably had little effect on potassium changes during exercise. 6. The changes in arterial plasma potassium during exercise are rapid and substantial. If transmitted to the extracellular fluid these changes would alter cell transmembrane potential and might as a result alter receptor sensitivity.

Relationship between Generation and Plasma Concentration of Anorganic Phosphorus. in Vivo Studies on Dialysis Patients and in Vitro Studies on Erythrocytes

1989 ◽  
Vol 12 (8) ◽  
pp. 524-532 ◽  
Author(s):  
H. Pogglitsch ◽  
W. Estelberger ◽  
W. Petek ◽  
S. Zitta ◽  
E. Ziak
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Concentration ◽  
Nonlinear Function ◽  
Extracellular Fluid ◽  
Red Cells ◽  
In Vitro Studies ◽  
In Vivo Studies

The plasma concentration of inorganic phosphorus (Pi) was determined before, during and after hemodialysis in 28 patients with chronic renal failure. Pi plasma concentration decreased rapidly when hemodialysis was started but did not fall below normal levels during continued dialysis. These changes of Pi concentration were fitted to a model of Pi kinetics in which Pi delivery to plasma is a nonlinear function of the extracellular Pi concentration. In separate in vitro studies, erythrocytes from six subjects with normal renal function and from 14 patients with chronic renal failure were incubated in homologous plasma with various amounts of Pi added. All other factors known to affect the Pi shift between intra - and extracellular fluid compartments (pH, calcium concentration) were kept constant. The relation between Pi concentration in plasma used for incubation and in red cells after 1h incubation suggested a mechanism in which a high plasma concentration results in movement of Pi into red cells where Pi is stored most probably in glucose esters. At low Pi plasma concentration Pi is delivered to plasma at a rate which cannot be explained solely by passive movement of intracellular Pi to plasma but requires additional generation from intracellular storage forms. The generation and delivery of Pi in patients and in their erythrocytes indicate a simple cell-mediated Pi homeostasis counter-acting abnormal fluctuations of plasma Pi.

scholarly journals The in Vitro Bleeding Time

1977 ◽  
Author(s):  
J.A. Blakely ◽  
M. F. X. Glynn ◽  
J. Prchal
Keyword(s):  
Whole Blood ◽  
Bleeding Time ◽  
Red Cells ◽  
Von Willebrand's Disease ◽  
Flow Rates ◽  
Shed Blood ◽  
Time Required ◽  
Teflon Tubing ◽  
Fibrin Thrombus

The observation by Didisheim of platelet-fibrin hemostatic plugs occluding puncture sites in teflon AV shunts prompted an attempt to produce similar plugs in vitro using a pump to circulate shed blood. Various anticoagulants, tubing types, flow rates, pressures and methods of producing suitable holes have been investigated. Satisfactory results have been obtained with drilled holes 0.013 - 0.018” diameter in tygon or teflon tubing using heparinized or native, but not EDTA or citrated whole blood. Holes are occluded by platelet fibrin thrombus. Red cells are necessary for plugs to form but are not a component of the plug. Time required for plugs to form correlate with the template bleeding time and are prolonged by thrombocytopenia, aspirin administration, and Von Willebrand’s disease. Possible applications are being explored.

scholarly journals CATION EXCHANGE BETWEEN CELLS AND PLASMA OF MAMMALIAN BLOOD

1951 ◽  
Vol 34 (4) ◽  
pp. 411-429 ◽  
Author(s):  
C. W. Sheppard ◽  
W. R. Martin ◽  
Gertrude Beyl
Keyword(s):  
Exchange Rate ◽  
Specific Activity ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Buffy Coat ◽  
Exponential Behavior ◽  
Compartment System ◽  
Mammalian Blood ◽  
Potassium Exchange ◽  
Sodium And Potassium

Sodium and potassium exchange has been studied in the blood of the sheep, dog, cow, and man. The potassium exchange rate in human cells is practically unaltered by increasing the plasma potassium concentration approximately threefold. Comparing the results in different species the exchange rate for potassium shows a rough correlation with the intracellular amount of the element. Expressed in per cent of the cellular content sodium tends to exchange more rapidly than potassium. In three instances the specific activity curves deviate from the simple exponential behavior of a two compartment system. In the exchange of potassium in canine blood the deviation is caused by the presence of a rapidly exchanging fraction in the buffy coat cells. Such an effect does not account for the inhomogeneity of sodium exchange in human blood.

In Vitro Assay of Platelet Adhesiveness with Washed and Tanned Human Red Cells

1968 ◽  
Vol 20 (03/04) ◽  
pp. 384-396 ◽  
Author(s):  
G Zbinden ◽  
S Tomlin
Keyword(s):  
Platelet Adhesion ◽  
Sodium Citrate ◽  
Blood Platelets ◽  
In Vitro Assay ◽  
Red Cells ◽  
Platelet Adhesiveness ◽  
Vitro Assay ◽  
In Vitro System ◽  
Human Red Cells

SummaryAn in vitro system is described in which adhesion of blood platelets to washed and tannic acid-treated red cells was assayed quantitatively by microscopic observation. ADP, epinephrine and TAME produced a reversible increase in platelet adhesiveness which was antagonized by AMP. With Evans blue, polyanetholsulfonate, phthalanilide NSC 38280, thrombin and heparin at concentrations above 1-4 u/ml the increase was irreversible. The ADP-induced increase in adhesiveness was inhibited by sodium citrate, EDTA, AMP, ATP and N-ethylmaleimide. EDTA, AMP and the SH-blocker N-ethylmaleimide also reduced spontaneous platelet adhesion to red cells. No significant effects were observed with adenosine, phenprocoumon, 5-HT, phthalanilide NSC 57155, various estrogens, progestogens and fatty acids, acetylsalicylic acid and similarly acting agents, hydroxylamine, glucose and KCN. The method may be useful for the screening of thrombogenic and antithrombotic properties of drugs.

LACK OF EFFECT OF CORTICOSTEROIDS ON THE IN VIVO DISAPPEARANCE OF SULFHYDRYL-INHIBITED AND ANTIBODY-COATED ERYTHROCYTES

1964 ◽  
Vol 47 (3_Suppl) ◽  
pp. S28-S36
Author(s):  
Kailash N. Agarwal
Keyword(s):  
Red Cells ◽  
List Type ◽  
Red Cell

ABSTRACT Red cells were incubated in vitro with sulfhydryl inhibitors and Rhantibody with and without prior incubation with prednisolone-hemisuccinate. These erythrocytes were labelled with Cr51 and P32 and their disappearance in vivo after autotransfusion was measured. Prior incubation with prednisolone-hemisuccinate had no effect on the rate of red cell disappearance. The disappearance of the cells was shown to take place without appreciable intravascular destruction.

scholarly journals Onset of acid-neutralizing action of a calcium/magnesium carbonate-based antacid using an artificial stomach model: an in vitro evaluation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Maxim Voropaiev ◽  
Deborah Nock
Keyword(s):  
In Vitro Study ◽  
Magnesium Carbonate ◽  
Human Gastrointestinal Tract ◽  
Pepsin Activity ◽  
Onset Of Action ◽  
Over The Counter ◽  
Calcium Magnesium ◽  
Secondary Objective ◽  
Time Required

Abstract Background Calcium carbonate antacids are potent over-the-counter antacids, made more effective by adding magnesium carbonate (as in Rennie, Bayer). However, published studies on their onset of action are scarce. Therefore, we carried out an in vitro study comparing Rennie and placebo under simulated conditions of the human stomach (artificial stomach model) to reconfirm the onset of action of Rennie. Methods The validated Simulator of the Human Intestinal Microbial Ecosystem apparatus (SHIME, ProDigest, Belgium) was used, comprising five reactors simulating different parts of the human gastrointestinal tract. Both Rennie and placebo were dosed at two tablets per incubation over six independent, 2-h stomach incubations each. Primary objectives: to evaluate the time required to achieve pH 3.0, 3.5, 4.0 and 4.5, as well as the maximum pH reached. Secondary objective: to evaluate pepsin activity over the entire 2-h gastric incubation. Results After addition of Rennie, the gastric medium reached a pH of 3.0 within 40 s. The maximum pH of 5.24 was maintained for almost 10 min. In contrast, the maximum pH with placebo was 1.28 during the entire gastric simulation. Furthermore, Rennie strongly reduced the activity of mucosa-damaging pepsin during the period of increased pH. With placebo, the lower pH resulted in consistently high loads of digested peptides, reflecting the high cumulative and instantaneous pepsin activity. Conclusions New data is a critical component in informed decision making. Our data confirm the high efficacy and fast onset of acid-neutralizing action of Rennie, which begins to work within seconds.

scholarly journals Entrapment of the Fastest Known Carbonic Anhydrase with Biomimetic Silica and Its Application for CO2 Sequestration

Polymers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 2452
Author(s):  
Chia-Jung Hsieh ◽  
Ju-Chuan Cheng ◽  
Chia-Jung Hu ◽  
Chi-Yang Yu
Keyword(s):  
Carbonic Anhydrase ◽  
High Activity ◽  
Co2 Sequestration ◽  
Residual Activity ◽  
Entrapment Efficiency ◽  
Free Form ◽  
Uncatalyzed Reaction ◽  
The Stability ◽  
Time Required

Capturing and storing CO2 is of prime importance. The rate of CO2 sequestration is often limited by the hydration of CO2, which can be greatly accelerated by using carbonic anhydrase (CA, EC 4.2.1.1) as a catalyst. In order to improve the stability and reusability of CA, a silica-condensing peptide (R5) was fused with the fastest known CA from Sulfurihydrogenibium azorense (SazCA) to form R5-SazCA; the fusion protein successfully performed in vitro silicification. The entrapment efficiency reached 100% and the silicified form (R5-SazCA-SP) showed a high activity recovery of 91%. The residual activity of R5-SazCA-SP was two-fold higher than that of the free form when stored at 25 °C for 35 days; R5-SazCA-SP still retained 86% of its activity after 10 cycles of reuse. Comparing with an uncatalyzed reaction, the time required for the onset of CaCO3 formation was shortened by 43% and 33% with the addition of R5-SazCA and R5-SazCA-SP, respectively. R5-SazCA-SP shows great potential as a robust and efficient biocatalyst for CO2 sequestration because of its high activity, high stability, and reusability.

Myocardial CO2 buffering: role of transmembrane transport of H+ or HCO3-ions

1976 ◽  
Vol 230 (4) ◽  
pp. 1037-1041 ◽  
Author(s):  
DR Strome ◽  
RL Clancy ◽  
NC Gonzalez
Keyword(s):  
Small Volume ◽  
Coronary Circulation ◽  
Myocardial Cell ◽  
Ringer Solution ◽  
Red Cells ◽  
Transmembrane Transport ◽  
High Degree

Isolated rabbit hearts were perfused with rabbit red cells suspended in Ringer solution. A small volume of perfusate was recirculated for 10 min at Pco2 of 33.4 +/- 0.9 or 150.8 +/- 7.5 mmHg. Hypercapnia resulted in an increase in perfusate HCO3- concentration that was smaller than that observed when isolated perfusate was equilibrated in vitro with the same CO2 tensions (delta HCO-3e = 1.6 mM, P less than 0.01). This difference is consistent with a net movement of HCO3- into or H+ out of the mycardial cell, and cannot be accounted for by dilution of HCO3- in the myocardial interstitium. Recirculation of perfusate through the coronary circulation at normal Pco2 for two consecutive 10-min periods was not followed by changes in perfusate HCO3- concentration. A high degree of correlation (r = 0.81) was observed between intracellular HCO-3e concentration and the corresponding delta HCO-3e in individual experiments. The results suggest that transmembrane exchange of H+ or HCO3- is a buffer mechanism for CO2 in the myocardial cell.

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