[Regulation of human erythrocyte volume. The role of calcium channels activated by calcium].

A mathematical model of stabilization of erythrocytes volume which takes into account the homeostasis of univalent ions and the calcium regulation of potassium flux through the membrane has been studied. The model has the only stable solution at all actual values of parameters. The investigation of the steady-state cell volume dependence on membrane permeability for potassium and sodium ions has shown that volume is much better protected against a nonspecific change in permeability than against a specific increase in the membrane permeability for potassium or sodium ions.

[Metabolic changes leading to oxidative lysis of erythrocytes maintained in a normal state in vitro].

It was shown that in vitro oxidative hemolysis of human erythrocytes occurs as a result of a great increase in membrane permeability to cations leading to osmotic damage of the cells. Infusion at a steady rate with a solution of tert-butylhydroperoxide in an erythrocyte suspension resulted in a rapid fall of the reduced glutathione level down to 0, when the rate of infusion exceeded the maximal rate of pentose phosphate pathway. Under these conditions the potassium ions liberation from the erythrocytes began with the drop of the reduced glutathione level down to zero, and the hemoglobin liberation - at the moment when more than 60% of potassium ions were liberated from the erythrocytes.

[Steady-state dependence of the methemoglobin reduction rate on its concentration in intact human erythrocytes].

The rate of methemoglobin reduction by the methemoglobin reductase system of intact human erythrocytes was measured as a rate of pyruvate formation in a quasi-steady state. Various methemoglobin concentrations (up to 100%) were generated by sodium nitrite additions. The steady state methemoglobin levels were maintained by infusion of a nitrite solution at a rate of 2.